TY  - JOUR
AU  - Bursać, Biljana
AU  - Bellachioma, Luisa
AU  - Gligorovska, Ljupka
AU  - Jovanović, Mirna
AU  - Teofilović, Ana
AU  - Vratarić, Miloš
AU  - Vojnović Milutinović, Danijela
AU  - Albacete, Alfonso
AU  - Martínez-Melgarejo, Purificación A
AU  - Morresi, Camilla
AU  - Damiani, Elisabetta
AU  - Bacchetti, Tiziana
AU  - Đorđević, Ana
PY  - 2024
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6533
AB  - Obesity is a pressing problem worldwide for which standard therapeutic strategies have limited effectiveness. The use of natural products seems to be a promising approach to alleviate obesity and its associated complications. The tepals of Crocus sativus plant, usually wasted in saffron production, are an unexplored source of bioactive compounds. Our aim was to elucidate the mechanisms of Crocus sativus (Cr) tepals extract in obesity by investigating its effects on adipocyte differentiation, visceral (VAT) and subcutaneous (SAT) adipose tissue hypertrophy, and lipid metabolism in an animal model of diet-induced obesity. To this end, mouse 3T3-F442A preadipocytes were treated with Cr tepals extract and the expression of adipocyte differentiation genes was determined. Caloric intake, body mass, triglycerides, systemic insulin sensitivity, histology, insulin signaling and lipid metabolism in VAT and SAT were analyzed in mice fed a 60% fat diet for 14 weeks and treated orally with Cr tepals extract during the last 5 weeks of the diet. We demonstrated for the first time that Cr tepals extract inhibits adipocyte differentiation in vitro. The animal model confirmed that oral treatment with Cr tepals extract results in weight loss, improved systemic insulin sensitivity, lower triglycerides, and improved lipid peroxidation. The suppressive effect of Cr tepals extract on adipocyte hypertrophy and inflammation was observed only in SAT, which, together with preserved SAT insulin signaling, most likely contributed to improved systemic insulin sensitivity. Our results suggest the functionality of SAT as a possible target for the treatment of obesity and its complications.
PB  - Hoboken: John Wiley and Sons
T2  - BioFactors
T1  - Crocus sativus tepals extract suppresses subcutaneous adipose tissue hypertrophy and improves systemic insulin sensitivity in mice on high-fat diet
DO  - 10.1002/biof.2043
ER  - 

@article{
author = "Bursać, Biljana and Bellachioma, Luisa and Gligorovska, Ljupka and Jovanović, Mirna and Teofilović, Ana and Vratarić, Miloš and Vojnović Milutinović, Danijela and Albacete, Alfonso and Martínez-Melgarejo, Purificación A and Morresi, Camilla and Damiani, Elisabetta and Bacchetti, Tiziana and Đorđević, Ana",
year = "2024",
abstract = "Obesity is a pressing problem worldwide for which standard therapeutic strategies have limited effectiveness. The use of natural products seems to be a promising approach to alleviate obesity and its associated complications. The tepals of Crocus sativus plant, usually wasted in saffron production, are an unexplored source of bioactive compounds. Our aim was to elucidate the mechanisms of Crocus sativus (Cr) tepals extract in obesity by investigating its effects on adipocyte differentiation, visceral (VAT) and subcutaneous (SAT) adipose tissue hypertrophy, and lipid metabolism in an animal model of diet-induced obesity. To this end, mouse 3T3-F442A preadipocytes were treated with Cr tepals extract and the expression of adipocyte differentiation genes was determined. Caloric intake, body mass, triglycerides, systemic insulin sensitivity, histology, insulin signaling and lipid metabolism in VAT and SAT were analyzed in mice fed a 60% fat diet for 14 weeks and treated orally with Cr tepals extract during the last 5 weeks of the diet. We demonstrated for the first time that Cr tepals extract inhibits adipocyte differentiation in vitro. The animal model confirmed that oral treatment with Cr tepals extract results in weight loss, improved systemic insulin sensitivity, lower triglycerides, and improved lipid peroxidation. The suppressive effect of Cr tepals extract on adipocyte hypertrophy and inflammation was observed only in SAT, which, together with preserved SAT insulin signaling, most likely contributed to improved systemic insulin sensitivity. Our results suggest the functionality of SAT as a possible target for the treatment of obesity and its complications.",
publisher = "Hoboken: John Wiley and Sons",
journal = "BioFactors",
title = "Crocus sativus tepals extract suppresses subcutaneous adipose tissue hypertrophy and improves systemic insulin sensitivity in mice on high-fat diet",
doi = "10.1002/biof.2043"
}

Bursać, B., Bellachioma, L., Gligorovska, L., Jovanović, M., Teofilović, A., Vratarić, M., Vojnović Milutinović, D., Albacete, A., Martínez-Melgarejo, P. A., Morresi, C., Damiani, E., Bacchetti, T.,& Đorđević, A.. (2024). Crocus sativus tepals extract suppresses subcutaneous adipose tissue hypertrophy and improves systemic insulin sensitivity in mice on high-fat diet. in BioFactors
Hoboken: John Wiley and Sons..
https://doi.org/10.1002/biof.2043

Bursać B, Bellachioma L, Gligorovska L, Jovanović M, Teofilović A, Vratarić M, Vojnović Milutinović D, Albacete A, Martínez-Melgarejo PA, Morresi C, Damiani E, Bacchetti T, Đorđević A. Crocus sativus tepals extract suppresses subcutaneous adipose tissue hypertrophy and improves systemic insulin sensitivity in mice on high-fat diet. in BioFactors. 2024;.
doi:10.1002/biof.2043 .

Bursać, Biljana, Bellachioma, Luisa, Gligorovska, Ljupka, Jovanović, Mirna, Teofilović, Ana, Vratarić, Miloš, Vojnović Milutinović, Danijela, Albacete, Alfonso, Martínez-Melgarejo, Purificación A, Morresi, Camilla, Damiani, Elisabetta, Bacchetti, Tiziana, Đorđević, Ana, "Crocus sativus tepals extract suppresses subcutaneous adipose tissue hypertrophy and improves systemic insulin sensitivity in mice on high-fat diet" in BioFactors (2024),
https://doi.org/10.1002/biof.2043 . .

TY  - JOUR
AU  - Bursać, Biljana
AU  - Bellachioma, Luisa
AU  - Gligorovska, Ljupka
AU  - Jovanović, Mirna
AU  - Teofilović, Ana
AU  - Vratarić, Miloš
AU  - Vojnović Milutinović, Danijela
AU  - Albacete, Alfonso
AU  - Martínez-Melgarejo, Purificación A
AU  - Morresi, Camilla
AU  - Damiani, Elisabetta
AU  - Bacchetti, Tiziana
AU  - Đorđević, Ana
PY  - 2024
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6532
AB  - Obesity is a pressing problem worldwide for which standard therapeutic strategies have limited effectiveness. The use of natural products seems to be a promising approach to alleviate obesity and its associated complications. The tepals of Crocus sativus plant, usually wasted in saffron production, are an unexplored source of bioactive compounds. Our aim was to elucidate the mechanisms of Crocus sativus (Cr) tepals extract in obesity by investigating its effects on adipocyte differentiation, visceral (VAT) and subcutaneous (SAT) adipose tissue hypertrophy, and lipid metabolism in an animal model of diet-induced obesity. To this end, mouse 3T3-F442A preadipocytes were treated with Cr tepals extract and the expression of adipocyte differentiation genes was determined. Caloric intake, body mass, triglycerides, systemic insulin sensitivity, histology, insulin signaling and lipid metabolism in VAT and SAT were analyzed in mice fed a 60% fat diet for 14 weeks and treated orally with Cr tepals extract during the last 5 weeks of the diet. We demonstrated for the first time that Cr tepals extract inhibits adipocyte differentiation in vitro. The animal model confirmed that oral treatment with Cr tepals extract results in weight loss, improved systemic insulin sensitivity, lower triglycerides, and improved lipid peroxidation. The suppressive effect of Cr tepals extract on adipocyte hypertrophy and inflammation was observed only in SAT, which, together with preserved SAT insulin signaling, most likely contributed to improved systemic insulin sensitivity. Our results suggest the functionality of SAT as a possible target for the treatment of obesity and its complications.
PB  - Hoboken: John Wiley and Sons
T2  - BioFactors
T1  - Crocus sativus tepals extract suppresses subcutaneous adipose tissue hypertrophy and improves systemic insulin sensitivity in mice on high-fat diet
DO  - 10.1002/biof.2043
ER  - 

@article{
author = "Bursać, Biljana and Bellachioma, Luisa and Gligorovska, Ljupka and Jovanović, Mirna and Teofilović, Ana and Vratarić, Miloš and Vojnović Milutinović, Danijela and Albacete, Alfonso and Martínez-Melgarejo, Purificación A and Morresi, Camilla and Damiani, Elisabetta and Bacchetti, Tiziana and Đorđević, Ana",
year = "2024",
abstract = "Obesity is a pressing problem worldwide for which standard therapeutic strategies have limited effectiveness. The use of natural products seems to be a promising approach to alleviate obesity and its associated complications. The tepals of Crocus sativus plant, usually wasted in saffron production, are an unexplored source of bioactive compounds. Our aim was to elucidate the mechanisms of Crocus sativus (Cr) tepals extract in obesity by investigating its effects on adipocyte differentiation, visceral (VAT) and subcutaneous (SAT) adipose tissue hypertrophy, and lipid metabolism in an animal model of diet-induced obesity. To this end, mouse 3T3-F442A preadipocytes were treated with Cr tepals extract and the expression of adipocyte differentiation genes was determined. Caloric intake, body mass, triglycerides, systemic insulin sensitivity, histology, insulin signaling and lipid metabolism in VAT and SAT were analyzed in mice fed a 60% fat diet for 14 weeks and treated orally with Cr tepals extract during the last 5 weeks of the diet. We demonstrated for the first time that Cr tepals extract inhibits adipocyte differentiation in vitro. The animal model confirmed that oral treatment with Cr tepals extract results in weight loss, improved systemic insulin sensitivity, lower triglycerides, and improved lipid peroxidation. The suppressive effect of Cr tepals extract on adipocyte hypertrophy and inflammation was observed only in SAT, which, together with preserved SAT insulin signaling, most likely contributed to improved systemic insulin sensitivity. Our results suggest the functionality of SAT as a possible target for the treatment of obesity and its complications.",
publisher = "Hoboken: John Wiley and Sons",
journal = "BioFactors",
title = "Crocus sativus tepals extract suppresses subcutaneous adipose tissue hypertrophy and improves systemic insulin sensitivity in mice on high-fat diet",
doi = "10.1002/biof.2043"
}

Bursać, B., Bellachioma, L., Gligorovska, L., Jovanović, M., Teofilović, A., Vratarić, M., Vojnović Milutinović, D., Albacete, A., Martínez-Melgarejo, P. A., Morresi, C., Damiani, E., Bacchetti, T.,& Đorđević, A.. (2024). Crocus sativus tepals extract suppresses subcutaneous adipose tissue hypertrophy and improves systemic insulin sensitivity in mice on high-fat diet. in BioFactors
Hoboken: John Wiley and Sons..
https://doi.org/10.1002/biof.2043

Bursać B, Bellachioma L, Gligorovska L, Jovanović M, Teofilović A, Vratarić M, Vojnović Milutinović D, Albacete A, Martínez-Melgarejo PA, Morresi C, Damiani E, Bacchetti T, Đorđević A. Crocus sativus tepals extract suppresses subcutaneous adipose tissue hypertrophy and improves systemic insulin sensitivity in mice on high-fat diet. in BioFactors. 2024;.
doi:10.1002/biof.2043 .

Bursać, Biljana, Bellachioma, Luisa, Gligorovska, Ljupka, Jovanović, Mirna, Teofilović, Ana, Vratarić, Miloš, Vojnović Milutinović, Danijela, Albacete, Alfonso, Martínez-Melgarejo, Purificación A, Morresi, Camilla, Damiani, Elisabetta, Bacchetti, Tiziana, Đorđević, Ana, "Crocus sativus tepals extract suppresses subcutaneous adipose tissue hypertrophy and improves systemic insulin sensitivity in mice on high-fat diet" in BioFactors (2024),
https://doi.org/10.1002/biof.2043 . .

TY  - CONF
AU  - Vratarić, Miloš
AU  - Teofilović, Ana
AU  - Vojnović Milutinović, Danijela
AU  - Veličković, Nataša
AU  - Bursać, Biljana
AU  - Gligorovska, Ljupka
AU  - Mićić, Bojana
AU  - Jovanović, Mirna
AU  - Đorđević, Ana
PY  - 2023
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6419
AB  - Introduction: High-fat diet primarily leads to obesity but it can also lead to obesity resistant (OR) phenotype
with various metabolic complications. Liver plays central role in modulating lipid metabolism in
response to dyslipidemia induced by adipose tissue hypertrophy. The aim of this study was to define key
regulatory points that adjust lipid metabolism in the liver of OR mice on high-fat diet (HFD).
Methods:Male C57BL/6J mice were divided into two groups: control group on normal diet (10 kcal% fat,
D12450J, Research Diets, USA) and HFD group (60 kcal% fat, D12492, Research Diets, USA). After 14 weeks,
mice on HFD were classified as obese or OR based on 30% difference in body weight gain compared
with controls. Liver sections were analyzed histologically, while alterations in hepatic lipid metabolism
were assessed by qPCR and Western blot.
Results: Although HFD restricted hepatic de novo lipogenesis, increased influx of free fatty acids (FFA)
led to accumulation of lipid droplets in the liver of obese mice. In OR mice, liver morphology was restored,
as was expression of insulin sensitive sterol regulatory element-binding protein 1c (SREBP-1c).
Level of FFA transporter CD36 was reduced, whereas higher expression of diacylglycerol acyltransferase
2 limited lipotoxicity in OR compared with obese mice. FFA β-oxidation remained unchanged in both
HFD groups.
Conclusion: Lower FFA input and reduced lipid storage and lipotoxicity in the liver of OR mice suggest
that dyslipidemic complications associated with obesity could be ameliorated by targeted modulation
of expression of FFA transporters and regulators of lipid droplet formation.
PB  - Belgrade: Institute of Molecular Genetics and Genetic Engineering, University of Belgrade
C3  - Abstract Book: CoMBoS2 - the Second Congress of Molecular Biologists of Serbia; 2023 Oct 6-8; Belgrade, Serbia
T1  - Modulation of hepatic lipid metabolism in obesity-resistant mice on a high-fat diet
SP  - 147
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6419
ER  - 

@conference{
author = "Vratarić, Miloš and Teofilović, Ana and Vojnović Milutinović, Danijela and Veličković, Nataša and Bursać, Biljana and Gligorovska, Ljupka and Mićić, Bojana and Jovanović, Mirna and Đorđević, Ana",
year = "2023",
abstract = "Introduction: High-fat diet primarily leads to obesity but it can also lead to obesity resistant (OR) phenotype
with various metabolic complications. Liver plays central role in modulating lipid metabolism in
response to dyslipidemia induced by adipose tissue hypertrophy. The aim of this study was to define key
regulatory points that adjust lipid metabolism in the liver of OR mice on high-fat diet (HFD).
Methods:Male C57BL/6J mice were divided into two groups: control group on normal diet (10 kcal% fat,
D12450J, Research Diets, USA) and HFD group (60 kcal% fat, D12492, Research Diets, USA). After 14 weeks,
mice on HFD were classified as obese or OR based on 30% difference in body weight gain compared
with controls. Liver sections were analyzed histologically, while alterations in hepatic lipid metabolism
were assessed by qPCR and Western blot.
Results: Although HFD restricted hepatic de novo lipogenesis, increased influx of free fatty acids (FFA)
led to accumulation of lipid droplets in the liver of obese mice. In OR mice, liver morphology was restored,
as was expression of insulin sensitive sterol regulatory element-binding protein 1c (SREBP-1c).
Level of FFA transporter CD36 was reduced, whereas higher expression of diacylglycerol acyltransferase
2 limited lipotoxicity in OR compared with obese mice. FFA β-oxidation remained unchanged in both
HFD groups.
Conclusion: Lower FFA input and reduced lipid storage and lipotoxicity in the liver of OR mice suggest
that dyslipidemic complications associated with obesity could be ameliorated by targeted modulation
of expression of FFA transporters and regulators of lipid droplet formation.",
publisher = "Belgrade: Institute of Molecular Genetics and Genetic Engineering, University of Belgrade",
journal = "Abstract Book: CoMBoS2 - the Second Congress of Molecular Biologists of Serbia; 2023 Oct 6-8; Belgrade, Serbia",
title = "Modulation of hepatic lipid metabolism in obesity-resistant mice on a high-fat diet",
pages = "147",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6419"
}

Vratarić, M., Teofilović, A., Vojnović Milutinović, D., Veličković, N., Bursać, B., Gligorovska, L., Mićić, B., Jovanović, M.,& Đorđević, A.. (2023). Modulation of hepatic lipid metabolism in obesity-resistant mice on a high-fat diet. in Abstract Book: CoMBoS2 - the Second Congress of Molecular Biologists of Serbia; 2023 Oct 6-8; Belgrade, Serbia
Belgrade: Institute of Molecular Genetics and Genetic Engineering, University of Belgrade., 147.
https://hdl.handle.net/21.15107/rcub_ibiss_6419

Vratarić M, Teofilović A, Vojnović Milutinović D, Veličković N, Bursać B, Gligorovska L, Mićić B, Jovanović M, Đorđević A. Modulation of hepatic lipid metabolism in obesity-resistant mice on a high-fat diet. in Abstract Book: CoMBoS2 - the Second Congress of Molecular Biologists of Serbia; 2023 Oct 6-8; Belgrade, Serbia. 2023;:147.
https://hdl.handle.net/21.15107/rcub_ibiss_6419 .

Vratarić, Miloš, Teofilović, Ana, Vojnović Milutinović, Danijela, Veličković, Nataša, Bursać, Biljana, Gligorovska, Ljupka, Mićić, Bojana, Jovanović, Mirna, Đorđević, Ana, "Modulation of hepatic lipid metabolism in obesity-resistant mice on a high-fat diet" in Abstract Book: CoMBoS2 - the Second Congress of Molecular Biologists of Serbia; 2023 Oct 6-8; Belgrade, Serbia (2023):147,
https://hdl.handle.net/21.15107/rcub_ibiss_6419 .

TY  - CONF
AU  - Brkljačić, Jelena
AU  - Veličković, Nataša
AU  - Vojnović-Milutinović, Danijela
AU  - Kovačević, Sanja
AU  - Teofilović, Ana
AU  - Bursać, Biljana
AU  - Pešić, Vesna
AU  - Đorđević, Ana
PY  - 2022
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5710
AB  - Фруктоза је прост шећер одувек присутан у људској исхрани. До 20. века људи су
путем воћа и поврћа уносили релативно ниске количине фруктозе, да би током 20.
века, након увођења високофруктозног кукурузног сирупа у прехрамбену
индустрију, дневни унос фруктозе био учетворостручен што је коинцидирало са
растућом преваленцијом метаболичких поремећаја. Ипак, новије студије показују
да преваленција метаболичких поремећаја и даље расте иако је дневни унос шећера
стабилан или се чак смањује, што указује на допринос других фактора, као што су
смањена физичка активност и свакодневна изложеност стресу. Наша истраживања
на животињском моделу пацова који је храњен фруктозом и хронично излаган
комбинацији стресора пружају одговор на питање да ли, и у којим ситуацијама,
фруктоза може да смањује штетне ефекте стреса, а у којим условима стрес
потенцира штетне ефекте фруктозе? Резултати показују да фруктоза, стрес и
њихова комбинација, на ткивно и полно специфичан начин утичу на метаболизам
глукозе и липида, као и на редокс и инфламаторни статус у јетри, скелетним
мишићима и висцералном масном ткиву, а да поред метаболичких ефеката
фруктоза и стрес утичу и на понашање животиња. Будући да ефекти фруктозе
зависе од дозе и патофизиолошког стања организма, енергија која од ње потиче се
може ефикасно складиштити и по потреби користити кроз физичку активност, док
сталан повећан унос фруктозе, уз седентарни начин живота и стрес може
допринети развоју метаболичких и кардиоваскуларних обољења.
AB  - Fruktoza je prost šećer oduvek prisutan u ljudskoj ishrani. Do 20. veka ljudi su putem voća i povrća unosili relativno niske količine fruktoze, da bi tokom 20. veka, nakon uvođenja visokofruktoznog kukuruznog sirupa u prehrambenu industriju, dnevni unos fruktoze bio učetvorostručen što je koincidiralo sa rastućom prevalencijom metaboličkih poremećaja. Ipak, novije studije pokazuju da prevalencija metaboličkih poremećaja i dalje raste iako je dnevni unos šećera stabilan ili se čak smanjuje, što ukazuje na doprinos drugih faktora, kao što su smanjena fizička aktivnost i svakodnevna izloženost stresu. Naša istraživanja na životinjskom modelu pacova koji je hranjen fruktozom i hronično izlagan kombinaciji stresora pružaju odgovor na pitanje da li, i u kojim situacijama, fruktoza može da smanjuje štetne efekte stresa, a u kojim uslovima stres potencira štetne efekte fruktoze? Rezultati pokazuju da fruktoza, stres i njihova kombinacija, na tkivno i polno specifičan način utiču na metabolizam glukoze i lipida, kao i na redoks i inflamatorni status u jetri, skeletnim mišićima i visceralnom masnom tkivu, a da pored metaboličkih efekata fruktoza i stres utiču i na ponašanje životinja. Budući da efekti fruktoze zavise od doze i patofiziološkog stanja organizma, energija koja od nje potiče se može efikasno skladištiti i po potrebi koristiti kroz fizičku aktivnost, dok stalan povećan unos fruktoze, uz sedentarni način života i stres može doprineti razvoju metaboličkih i kardiovaskularnih oboljenja.
PB  - Belgrade: Serbian Biological Society
C3  - Knjiga sažetaka: Treći Kongres biologa Srbije: Osnovna i primenjena istraživanja: Metodika nastave; 2022 Sep 21-25; Zlatibor, Serbia
T1  - Fruktoza u ishrani: Ima li razloga za zabrinutost?
T1  - Фруктоза у исхрани: Има ли разлога за забринутост?
SP  - 284
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5710
ER  - 

@conference{
author = "Brkljačić, Jelena and Veličković, Nataša and Vojnović-Milutinović, Danijela and Kovačević, Sanja and Teofilović, Ana and Bursać, Biljana and Pešić, Vesna and Đorđević, Ana",
year = "2022",
abstract = "Фруктоза је прост шећер одувек присутан у људској исхрани. До 20. века људи су
путем воћа и поврћа уносили релативно ниске количине фруктозе, да би током 20.
века, након увођења високофруктозног кукурузног сирупа у прехрамбену
индустрију, дневни унос фруктозе био учетворостручен што је коинцидирало са
растућом преваленцијом метаболичких поремећаја. Ипак, новије студије показују
да преваленција метаболичких поремећаја и даље расте иако је дневни унос шећера
стабилан или се чак смањује, што указује на допринос других фактора, као што су
смањена физичка активност и свакодневна изложеност стресу. Наша истраживања
на животињском моделу пацова који је храњен фруктозом и хронично излаган
комбинацији стресора пружају одговор на питање да ли, и у којим ситуацијама,
фруктоза може да смањује штетне ефекте стреса, а у којим условима стрес
потенцира штетне ефекте фруктозе? Резултати показују да фруктоза, стрес и
њихова комбинација, на ткивно и полно специфичан начин утичу на метаболизам
глукозе и липида, као и на редокс и инфламаторни статус у јетри, скелетним
мишићима и висцералном масном ткиву, а да поред метаболичких ефеката
фруктоза и стрес утичу и на понашање животиња. Будући да ефекти фруктозе
зависе од дозе и патофизиолошког стања организма, енергија која од ње потиче се
може ефикасно складиштити и по потреби користити кроз физичку активност, док
сталан повећан унос фруктозе, уз седентарни начин живота и стрес може
допринети развоју метаболичких и кардиоваскуларних обољења., Fruktoza je prost šećer oduvek prisutan u ljudskoj ishrani. Do 20. veka ljudi su putem voća i povrća unosili relativno niske količine fruktoze, da bi tokom 20. veka, nakon uvođenja visokofruktoznog kukuruznog sirupa u prehrambenu industriju, dnevni unos fruktoze bio učetvorostručen što je koincidiralo sa rastućom prevalencijom metaboličkih poremećaja. Ipak, novije studije pokazuju da prevalencija metaboličkih poremećaja i dalje raste iako je dnevni unos šećera stabilan ili se čak smanjuje, što ukazuje na doprinos drugih faktora, kao što su smanjena fizička aktivnost i svakodnevna izloženost stresu. Naša istraživanja na životinjskom modelu pacova koji je hranjen fruktozom i hronično izlagan kombinaciji stresora pružaju odgovor na pitanje da li, i u kojim situacijama, fruktoza može da smanjuje štetne efekte stresa, a u kojim uslovima stres potencira štetne efekte fruktoze? Rezultati pokazuju da fruktoza, stres i njihova kombinacija, na tkivno i polno specifičan način utiču na metabolizam glukoze i lipida, kao i na redoks i inflamatorni status u jetri, skeletnim mišićima i visceralnom masnom tkivu, a da pored metaboličkih efekata fruktoza i stres utiču i na ponašanje životinja. Budući da efekti fruktoze zavise od doze i patofiziološkog stanja organizma, energija koja od nje potiče se može efikasno skladištiti i po potrebi koristiti kroz fizičku aktivnost, dok stalan povećan unos fruktoze, uz sedentarni način života i stres može doprineti razvoju metaboličkih i kardiovaskularnih oboljenja.",
publisher = "Belgrade: Serbian Biological Society",
journal = "Knjiga sažetaka: Treći Kongres biologa Srbije: Osnovna i primenjena istraživanja: Metodika nastave; 2022 Sep 21-25; Zlatibor, Serbia",
title = "Fruktoza u ishrani: Ima li razloga za zabrinutost?, Фруктоза у исхрани: Има ли разлога за забринутост?",
pages = "284",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5710"
}

Brkljačić, J., Veličković, N., Vojnović-Milutinović, D., Kovačević, S., Teofilović, A., Bursać, B., Pešić, V.,& Đorđević, A.. (2022). Fruktoza u ishrani: Ima li razloga za zabrinutost?. in Knjiga sažetaka: Treći Kongres biologa Srbije: Osnovna i primenjena istraživanja: Metodika nastave; 2022 Sep 21-25; Zlatibor, Serbia
Belgrade: Serbian Biological Society., 284.
https://hdl.handle.net/21.15107/rcub_ibiss_5710

Brkljačić J, Veličković N, Vojnović-Milutinović D, Kovačević S, Teofilović A, Bursać B, Pešić V, Đorđević A. Fruktoza u ishrani: Ima li razloga za zabrinutost?. in Knjiga sažetaka: Treći Kongres biologa Srbije: Osnovna i primenjena istraživanja: Metodika nastave; 2022 Sep 21-25; Zlatibor, Serbia. 2022;:284.
https://hdl.handle.net/21.15107/rcub_ibiss_5710 .

Brkljačić, Jelena, Veličković, Nataša, Vojnović-Milutinović, Danijela, Kovačević, Sanja, Teofilović, Ana, Bursać, Biljana, Pešić, Vesna, Đorđević, Ana, "Fruktoza u ishrani: Ima li razloga za zabrinutost?" in Knjiga sažetaka: Treći Kongres biologa Srbije: Osnovna i primenjena istraživanja: Metodika nastave; 2022 Sep 21-25; Zlatibor, Serbia (2022):284,
https://hdl.handle.net/21.15107/rcub_ibiss_5710 .

TY  - JOUR
AU  - Sirif, Zidane Abdulbaset
AU  - Kovačević, Sanja
AU  - Bursać, Biljana
AU  - Lakić, Iva
AU  - Veličković, Nataša
AU  - Jevđović, Tanja
AU  - Đorđević, Ana
PY  - 2022
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5024
AB  - Appetite regulation in the hypothalamus is dependent on
hormonal signals from the periphery, such as insulin and
leptin, and can be modulated by both sugar-rich diet and
stress. Our aim was to explore the effects of 9-week feeding
with 20% fructose solution combined with 4-week
chronic unpredictable stress, on appetite-regulating neuropeptides
and modulatory role of leptin and insulin signalling
in the hypothalamus of male Wistar rats. Energy
intake, body mass and adiposity, as well as circulatory
leptin and insulin concentrations were assessed. Hypothalamic
insulin signalling was analysed at the level of glucose
transporters, as well as at the protein level and phosphorylation
of insulin receptor, insulin receptor supstrate-1, Akt
and ERK. Phosphorylation of AMP-activated protein kinase
(AMPK), level of protein tyrosine phosphatase 1B (PTP1B)
and expression of leptin receptor (ObRb) and suppressor of
cytokine signalling 3 (SOCS3) were also analysed, together
with the expression of orexigenic agouti-related protein
(AgRP) and anorexigenic proopiomelanocortin (POMC) neuropeptides.
The results revealed that stress decreased body
mass and adiposity, blood leptin level and expression of
ObRb, SOCS3 and POMC, while combination with fructose
diet led to marked increase of AgRP, associated with AMPK
phosphorylation despite increased plasma insulin. Reduced
Akt, enhanced ERK activity and elevated PTP1B were also
observed in the hypothalamus of these animals. In conclusion,
our results showed that joint effects of fructose diet
and stress are more deleterious than the separate ones,
since inappropriate appetite control in the hypothalamus
may provide a setting for the disturbed energy homeostasis
in the long run.
PB  - Warsaw: Polish Biochemical Society
T2  - Acta Biochimica Polonica
T1  - Combination of chronic stress with fructose diet increases AMPactivated protein kinase phosphorylation and affects agoutirelated protein and proopiomelanocortin expression in the hypothalamus of male Wistar rats
IS  - 6075
DO  - 10.18388/abp.2020_6075
ER  - 

@article{
author = "Sirif, Zidane Abdulbaset and Kovačević, Sanja and Bursać, Biljana and Lakić, Iva and Veličković, Nataša and Jevđović, Tanja and Đorđević, Ana",
year = "2022",
abstract = "Appetite regulation in the hypothalamus is dependent on
hormonal signals from the periphery, such as insulin and
leptin, and can be modulated by both sugar-rich diet and
stress. Our aim was to explore the effects of 9-week feeding
with 20% fructose solution combined with 4-week
chronic unpredictable stress, on appetite-regulating neuropeptides
and modulatory role of leptin and insulin signalling
in the hypothalamus of male Wistar rats. Energy
intake, body mass and adiposity, as well as circulatory
leptin and insulin concentrations were assessed. Hypothalamic
insulin signalling was analysed at the level of glucose
transporters, as well as at the protein level and phosphorylation
of insulin receptor, insulin receptor supstrate-1, Akt
and ERK. Phosphorylation of AMP-activated protein kinase
(AMPK), level of protein tyrosine phosphatase 1B (PTP1B)
and expression of leptin receptor (ObRb) and suppressor of
cytokine signalling 3 (SOCS3) were also analysed, together
with the expression of orexigenic agouti-related protein
(AgRP) and anorexigenic proopiomelanocortin (POMC) neuropeptides.
The results revealed that stress decreased body
mass and adiposity, blood leptin level and expression of
ObRb, SOCS3 and POMC, while combination with fructose
diet led to marked increase of AgRP, associated with AMPK
phosphorylation despite increased plasma insulin. Reduced
Akt, enhanced ERK activity and elevated PTP1B were also
observed in the hypothalamus of these animals. In conclusion,
our results showed that joint effects of fructose diet
and stress are more deleterious than the separate ones,
since inappropriate appetite control in the hypothalamus
may provide a setting for the disturbed energy homeostasis
in the long run.",
publisher = "Warsaw: Polish Biochemical Society",
journal = "Acta Biochimica Polonica",
title = "Combination of chronic stress with fructose diet increases AMPactivated protein kinase phosphorylation and affects agoutirelated protein and proopiomelanocortin expression in the hypothalamus of male Wistar rats",
number = "6075",
doi = "10.18388/abp.2020_6075"
}

Sirif, Z. A., Kovačević, S., Bursać, B., Lakić, I., Veličković, N., Jevđović, T.,& Đorđević, A.. (2022). Combination of chronic stress with fructose diet increases AMPactivated protein kinase phosphorylation and affects agoutirelated protein and proopiomelanocortin expression in the hypothalamus of male Wistar rats. in Acta Biochimica Polonica
Warsaw: Polish Biochemical Society.(6075).
https://doi.org/10.18388/abp.2020_6075

Sirif ZA, Kovačević S, Bursać B, Lakić I, Veličković N, Jevđović T, Đorđević A. Combination of chronic stress with fructose diet increases AMPactivated protein kinase phosphorylation and affects agoutirelated protein and proopiomelanocortin expression in the hypothalamus of male Wistar rats. in Acta Biochimica Polonica. 2022;(6075).
doi:10.18388/abp.2020_6075 .

Sirif, Zidane Abdulbaset, Kovačević, Sanja, Bursać, Biljana, Lakić, Iva, Veličković, Nataša, Jevđović, Tanja, Đorđević, Ana, "Combination of chronic stress with fructose diet increases AMPactivated protein kinase phosphorylation and affects agoutirelated protein and proopiomelanocortin expression in the hypothalamus of male Wistar rats" in Acta Biochimica Polonica, no. 6075 (2022),
https://doi.org/10.18388/abp.2020_6075 . .

TY  - JOUR
AU  - Vratarić, Miloš
AU  - Šenk, Vladimir
AU  - Bursać, Biljana
AU  - Gligorovska, Ljupka
AU  - Ignjatović, Đurđica
AU  - Kovačević, Sanja
AU  - Veličković, Nataša
AU  - Đorđević, Ana
PY  - 2021
UR  - https://onlinelibrary.wiley.com/doi/10.1002/biof.1802
UR  - http://www.ncbi.nlm.nih.gov/pubmed/34767656
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/4687
AB  - Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine that represents a link between diet-induced inflammation and insulin resistance. Our aim was to examine whether fructose diet affects inflammation and insulin signaling in the prefrontal cortex (PFC) of Mif knockout mice (MIF-KO), and their possible link to neural plasticity and behavior. We analyzed nuclear factor κB (NF-κB) and glucocorticoid signaling, expression of F4/80, IL-1β, TNF-α, TLR-4, MyD88, arginase 1 (Arg-1), mannose receptor (Mrc-1), and leukemia inhibitory factor (Lif) to assess inflammation in the PFC of C57/BL6J and MIF-KO mice consuming 20% fructose solution for 9 weeks. Insulin receptor (IR), IRS-1 serine phosphorylations (307 and 1101) and activity of PKCα, Akt, GSK-3β and AMPKα were used to analyze insulin signaling. Brain-derived neurotrophic factor (BDNF) and insulin-like growth factor 1 (IGF-1) mRNA levels, together with synapthophysin and PSD-95 protein level and calcium calmodulin-dependent kinase 2 (CaMKII) activity, were used as plasticity markers. Behavior was examined in elevated plus maze, light dark box and novel object recognition test. The results showed concomitant increase of Tnf-α, Tlr-4, MyD88 and M2 microglia markers (Arg-1, Mrc-1, Lif) in the PFC of MIF-KO, paralleled with unchanged glucocorticoid and insulin signaling. Increase of BDNF and IGF-1 was paralleled with increased CaMKII activity, decreased PSD-95 protein level, anxiogenic behavior, and impaired memory in MIF-KO mice. Fructose feeding restored these parameters in the PFC to the control level and mitigated behavioral changes, suggesting that ameliorating effects of fructose on neuroinflammation and behavior depend on the presence of MIF.
T2  - BioFactors (Oxford, England)
T1  - Fructose diet ameliorates effects of macrophage migration inhibitory factor deficiency on prefrontal cortex inflammation, neural plasticity, and behavior in male mice.
DO  - 10.1002/biof.1802
ER  - 

@article{
author = "Vratarić, Miloš and Šenk, Vladimir and Bursać, Biljana and Gligorovska, Ljupka and Ignjatović, Đurđica and Kovačević, Sanja and Veličković, Nataša and Đorđević, Ana",
year = "2021",
abstract = "Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine that represents a link between diet-induced inflammation and insulin resistance. Our aim was to examine whether fructose diet affects inflammation and insulin signaling in the prefrontal cortex (PFC) of Mif knockout mice (MIF-KO), and their possible link to neural plasticity and behavior. We analyzed nuclear factor κB (NF-κB) and glucocorticoid signaling, expression of F4/80, IL-1β, TNF-α, TLR-4, MyD88, arginase 1 (Arg-1), mannose receptor (Mrc-1), and leukemia inhibitory factor (Lif) to assess inflammation in the PFC of C57/BL6J and MIF-KO mice consuming 20% fructose solution for 9 weeks. Insulin receptor (IR), IRS-1 serine phosphorylations (307 and 1101) and activity of PKCα, Akt, GSK-3β and AMPKα were used to analyze insulin signaling. Brain-derived neurotrophic factor (BDNF) and insulin-like growth factor 1 (IGF-1) mRNA levels, together with synapthophysin and PSD-95 protein level and calcium calmodulin-dependent kinase 2 (CaMKII) activity, were used as plasticity markers. Behavior was examined in elevated plus maze, light dark box and novel object recognition test. The results showed concomitant increase of Tnf-α, Tlr-4, MyD88 and M2 microglia markers (Arg-1, Mrc-1, Lif) in the PFC of MIF-KO, paralleled with unchanged glucocorticoid and insulin signaling. Increase of BDNF and IGF-1 was paralleled with increased CaMKII activity, decreased PSD-95 protein level, anxiogenic behavior, and impaired memory in MIF-KO mice. Fructose feeding restored these parameters in the PFC to the control level and mitigated behavioral changes, suggesting that ameliorating effects of fructose on neuroinflammation and behavior depend on the presence of MIF.",
journal = "BioFactors (Oxford, England)",
title = "Fructose diet ameliorates effects of macrophage migration inhibitory factor deficiency on prefrontal cortex inflammation, neural plasticity, and behavior in male mice.",
doi = "10.1002/biof.1802"
}

Vratarić, M., Šenk, V., Bursać, B., Gligorovska, L., Ignjatović, Đ., Kovačević, S., Veličković, N.,& Đorđević, A.. (2021). Fructose diet ameliorates effects of macrophage migration inhibitory factor deficiency on prefrontal cortex inflammation, neural plasticity, and behavior in male mice.. in BioFactors (Oxford, England).
https://doi.org/10.1002/biof.1802

Vratarić M, Šenk V, Bursać B, Gligorovska L, Ignjatović Đ, Kovačević S, Veličković N, Đorđević A. Fructose diet ameliorates effects of macrophage migration inhibitory factor deficiency on prefrontal cortex inflammation, neural plasticity, and behavior in male mice.. in BioFactors (Oxford, England). 2021;.
doi:10.1002/biof.1802 .

Vratarić, Miloš, Šenk, Vladimir, Bursać, Biljana, Gligorovska, Ljupka, Ignjatović, Đurđica, Kovačević, Sanja, Veličković, Nataša, Đorđević, Ana, "Fructose diet ameliorates effects of macrophage migration inhibitory factor deficiency on prefrontal cortex inflammation, neural plasticity, and behavior in male mice." in BioFactors (Oxford, England) (2021),
https://doi.org/10.1002/biof.1802 . .

TY  - JOUR
AU  - Kovačević, Sanja
AU  - Brkljačić, Jelena
AU  - Vojnović-Milutinović, Danijela
AU  - Gligorovska, Ljupka
AU  - Bursać, Biljana
AU  - Elaković, Ivana
AU  - Đorđević, Ana
PY  - 2021
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/4705
AB  - Introduction: Obesity and related metabolic disturbances are frequently related to
modern lifestyle and are characterized by excessive fructose intake. Visceral adipose
tissue (VAT) inflammation has a central role in the development of insulin resistance, type
2 diabetes (T2D), and metabolic syndrome. Since sex-related differences in susceptibility
and progression of metabolic disorders are not yet fully understood, our aim was to
examine inflammation and insulin signaling in VAT of fructose-fed female and male
adult rats.
Methods: We analyzed effects of 9-week 10% fructose-enriched diet on energy intake,
VATmass and histology, and systemic insulin sensitivity. VAT insulin signaling andmarkers
of VAT inflammation, and antioxidative defense status were also evaluated.
Results: The fructose diet had no effect on VAT mass and systemic insulin signaling
in the female and male rats, while it raised plasma uric acid, increased PPARg level in
the VAT, and initiated the development of a distinctive population of small adipocytes
in the females. Also, adipose tissue insulin resistance, evidenced by increased PTP1B
and insulin receptor substrate 1 (IRS1) inhibitory phosphorylation and decreased Akt
activity, was detected. In addition, fructose stimulated the nuclear accumulation of NFkB,
increased expression of proinflammatory cytokines (IL-1b, IL-6, and TNFα), and protein
level of macrophage marker F4/80, superoxide dismutase 1, and glutathione reductase.
In contrast to the females, the fructose diet had no effect on plasma uric acid and
VAT inflammation in the male rats, but less prominent alterations in VAT insulin signaling
were observed.
Conclusion: Even though dietary fructose did not elicit changes in energy intake and
led to obesity in the females, it initiated the proliferation of small-sized adipocytes capable
of storing fats further. In contrast to the males, this state of VAT was accompanied
with enhanced inflammation, which most likely contributed to the development of insulin
resistance. The observed distinction could possibly originate from sex-related differences
in uric acid metabolism. Our results suggest that VAT inflammation could precede obesity and start even before the measurable increase in VAT mass, making it a silent risk factor
for the development of T2D. Our results emphasize that adipose tissue dysfunction,
rather than its simple enlargement, could significantly contribute to the onset and
development of obesity and related metabolic disorders.
PB  - Lausanne: Frontiers Media SA
T2  - Frontiers in Nutrition
T1  - Fructose Induces Visceral Adipose Tissue Inflammation and Insulin Resistance Even Without Development of Obesity in Adult Female but Not in Male Rats
VL  - 8
DO  - 10.3389/fnut.2021.749328
SP  - 749328
ER  - 

@article{
author = "Kovačević, Sanja and Brkljačić, Jelena and Vojnović-Milutinović, Danijela and Gligorovska, Ljupka and Bursać, Biljana and Elaković, Ivana and Đorđević, Ana",
year = "2021",
abstract = "Introduction: Obesity and related metabolic disturbances are frequently related to
modern lifestyle and are characterized by excessive fructose intake. Visceral adipose
tissue (VAT) inflammation has a central role in the development of insulin resistance, type
2 diabetes (T2D), and metabolic syndrome. Since sex-related differences in susceptibility
and progression of metabolic disorders are not yet fully understood, our aim was to
examine inflammation and insulin signaling in VAT of fructose-fed female and male
adult rats.
Methods: We analyzed effects of 9-week 10% fructose-enriched diet on energy intake,
VATmass and histology, and systemic insulin sensitivity. VAT insulin signaling andmarkers
of VAT inflammation, and antioxidative defense status were also evaluated.
Results: The fructose diet had no effect on VAT mass and systemic insulin signaling
in the female and male rats, while it raised plasma uric acid, increased PPARg level in
the VAT, and initiated the development of a distinctive population of small adipocytes
in the females. Also, adipose tissue insulin resistance, evidenced by increased PTP1B
and insulin receptor substrate 1 (IRS1) inhibitory phosphorylation and decreased Akt
activity, was detected. In addition, fructose stimulated the nuclear accumulation of NFkB,
increased expression of proinflammatory cytokines (IL-1b, IL-6, and TNFα), and protein
level of macrophage marker F4/80, superoxide dismutase 1, and glutathione reductase.
In contrast to the females, the fructose diet had no effect on plasma uric acid and
VAT inflammation in the male rats, but less prominent alterations in VAT insulin signaling
were observed.
Conclusion: Even though dietary fructose did not elicit changes in energy intake and
led to obesity in the females, it initiated the proliferation of small-sized adipocytes capable
of storing fats further. In contrast to the males, this state of VAT was accompanied
with enhanced inflammation, which most likely contributed to the development of insulin
resistance. The observed distinction could possibly originate from sex-related differences
in uric acid metabolism. Our results suggest that VAT inflammation could precede obesity and start even before the measurable increase in VAT mass, making it a silent risk factor
for the development of T2D. Our results emphasize that adipose tissue dysfunction,
rather than its simple enlargement, could significantly contribute to the onset and
development of obesity and related metabolic disorders.",
publisher = "Lausanne: Frontiers Media SA",
journal = "Frontiers in Nutrition",
title = "Fructose Induces Visceral Adipose Tissue Inflammation and Insulin Resistance Even Without Development of Obesity in Adult Female but Not in Male Rats",
volume = "8",
doi = "10.3389/fnut.2021.749328",
pages = "749328"
}

Kovačević, S., Brkljačić, J., Vojnović-Milutinović, D., Gligorovska, L., Bursać, B., Elaković, I.,& Đorđević, A.. (2021). Fructose Induces Visceral Adipose Tissue Inflammation and Insulin Resistance Even Without Development of Obesity in Adult Female but Not in Male Rats. in Frontiers in Nutrition
Lausanne: Frontiers Media SA., 8, 749328.
https://doi.org/10.3389/fnut.2021.749328

Kovačević S, Brkljačić J, Vojnović-Milutinović D, Gligorovska L, Bursać B, Elaković I, Đorđević A. Fructose Induces Visceral Adipose Tissue Inflammation and Insulin Resistance Even Without Development of Obesity in Adult Female but Not in Male Rats. in Frontiers in Nutrition. 2021;8:749328.
doi:10.3389/fnut.2021.749328 .

Kovačević, Sanja, Brkljačić, Jelena, Vojnović-Milutinović, Danijela, Gligorovska, Ljupka, Bursać, Biljana, Elaković, Ivana, Đorđević, Ana, "Fructose Induces Visceral Adipose Tissue Inflammation and Insulin Resistance Even Without Development of Obesity in Adult Female but Not in Male Rats" in Frontiers in Nutrition, 8 (2021):749328,
https://doi.org/10.3389/fnut.2021.749328 . .

TY  - JOUR
AU  - Vratarić, Miloš
AU  - Šenk, Vladimir
AU  - Bursać, Biljana
AU  - Gligorovska, Ljupka
AU  - Ignjatović, Đurđica
AU  - Kovačević, Sanja
AU  - Veličković, Nataša
AU  - Đorđević, Ana
PY  - 2021
UR  - https://onlinelibrary.wiley.com/doi/10.1002/biof.1802
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/4773
AB  - Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine that represents a link between diet-induced inflammation and insulin resistance. Our aim was to examine whether fructose diet affects inflammation and insulin signaling in the prefrontal cortex (PFC) of Mif knockout mice (MIF-KO), and their possible link to neural plasticity and behavior. We analyzed nuclear factor κB (NF-κB) and glucocorticoid signaling, expression of F4/80, IL-1β, TNF-α, TLR-4, MyD88, arginase 1 (Arg-1), mannose receptor (Mrc-1), and leukemia inhibitory factor (Lif) to assess inflammation in the PFC of C57/BL6J and MIF-KO mice consuming 20% fructose solution for 9 weeks. Insulin receptor (IR), IRS-1 serine phosphorylations (307 and 1101) and activity of PKCα, Akt, GSK-3β and AMPKα were used to analyze insulin signaling. Brain-derived neurotrophic factor (BDNF) and insulin-like growth factor 1 (IGF-1) mRNA levels, together with synapthophysin and PSD-95 protein level and calcium calmodulin-dependent kinase 2 (CaMKII) activity, were used as plasticity markers. Behavior was examined in elevated plus maze, light dark box and novel object recognition test. The results showed concomitant increase of Tnf-α, Tlr-4, MyD88 and M2 microglia markers (Arg-1, Mrc-1, Lif) in the PFC of MIF-KO, paralleled with unchanged glucocorticoid and insulin signaling. Increase of BDNF and IGF-1 was paralleled with increased CaMKII activity, decreased PSD-95 protein level, anxiogenic behavior, and impaired memory in MIF-KO mice. Fructose feeding restored these parameters in the PFC to the control level and mitigated behavioral changes, suggesting that ameliorating effects of fructose on neuroinflammation and behavior depend on the presence of MIF.
T2  - BioFactors (Oxford, England)
T1  - Fructose diet ameliorates effects of macrophage migration inhibitory factor deficiency on prefrontal cortex inflammation, neural plasticity, and behavior in male mice.
DO  - 10.1002/biof.1802
ER  - 

@article{
author = "Vratarić, Miloš and Šenk, Vladimir and Bursać, Biljana and Gligorovska, Ljupka and Ignjatović, Đurđica and Kovačević, Sanja and Veličković, Nataša and Đorđević, Ana",
year = "2021",
abstract = "Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine that represents a link between diet-induced inflammation and insulin resistance. Our aim was to examine whether fructose diet affects inflammation and insulin signaling in the prefrontal cortex (PFC) of Mif knockout mice (MIF-KO), and their possible link to neural plasticity and behavior. We analyzed nuclear factor κB (NF-κB) and glucocorticoid signaling, expression of F4/80, IL-1β, TNF-α, TLR-4, MyD88, arginase 1 (Arg-1), mannose receptor (Mrc-1), and leukemia inhibitory factor (Lif) to assess inflammation in the PFC of C57/BL6J and MIF-KO mice consuming 20% fructose solution for 9 weeks. Insulin receptor (IR), IRS-1 serine phosphorylations (307 and 1101) and activity of PKCα, Akt, GSK-3β and AMPKα were used to analyze insulin signaling. Brain-derived neurotrophic factor (BDNF) and insulin-like growth factor 1 (IGF-1) mRNA levels, together with synapthophysin and PSD-95 protein level and calcium calmodulin-dependent kinase 2 (CaMKII) activity, were used as plasticity markers. Behavior was examined in elevated plus maze, light dark box and novel object recognition test. The results showed concomitant increase of Tnf-α, Tlr-4, MyD88 and M2 microglia markers (Arg-1, Mrc-1, Lif) in the PFC of MIF-KO, paralleled with unchanged glucocorticoid and insulin signaling. Increase of BDNF and IGF-1 was paralleled with increased CaMKII activity, decreased PSD-95 protein level, anxiogenic behavior, and impaired memory in MIF-KO mice. Fructose feeding restored these parameters in the PFC to the control level and mitigated behavioral changes, suggesting that ameliorating effects of fructose on neuroinflammation and behavior depend on the presence of MIF.",
journal = "BioFactors (Oxford, England)",
title = "Fructose diet ameliorates effects of macrophage migration inhibitory factor deficiency on prefrontal cortex inflammation, neural plasticity, and behavior in male mice.",
doi = "10.1002/biof.1802"
}

Vratarić, M., Šenk, V., Bursać, B., Gligorovska, L., Ignjatović, Đ., Kovačević, S., Veličković, N.,& Đorđević, A.. (2021). Fructose diet ameliorates effects of macrophage migration inhibitory factor deficiency on prefrontal cortex inflammation, neural plasticity, and behavior in male mice.. in BioFactors (Oxford, England).
https://doi.org/10.1002/biof.1802

Vratarić M, Šenk V, Bursać B, Gligorovska L, Ignjatović Đ, Kovačević S, Veličković N, Đorđević A. Fructose diet ameliorates effects of macrophage migration inhibitory factor deficiency on prefrontal cortex inflammation, neural plasticity, and behavior in male mice.. in BioFactors (Oxford, England). 2021;.
doi:10.1002/biof.1802 .

Vratarić, Miloš, Šenk, Vladimir, Bursać, Biljana, Gligorovska, Ljupka, Ignjatović, Đurđica, Kovačević, Sanja, Veličković, Nataša, Đorđević, Ana, "Fructose diet ameliorates effects of macrophage migration inhibitory factor deficiency on prefrontal cortex inflammation, neural plasticity, and behavior in male mice." in BioFactors (Oxford, England) (2021),
https://doi.org/10.1002/biof.1802 . .

TY  - JOUR
AU  - Vojnović-Milutinović, Danijela
AU  - Brkljačić, Jelena
AU  - Teofilović, Ana
AU  - Bursać, Biljana
AU  - Radovanović, Marina
AU  - Gligorovska, Ljupka
AU  - Kovačević, Sanja
AU  - Đorđević, Ana
AU  - Preitner, Frederic
AU  - Tappy, Luc
AU  - Matić, Gordana
AU  - Veličković, Nataša
PY  - 2020
UR  - https://onlinelibrary.wiley.com/doi/abs/10.1002/mnfr.201901141
UR  - http://www.ncbi.nlm.nih.gov/pubmed/32379936
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3702
AB  - SCOPE Intake of fructose-sweetened beverages and chronic stress (CS) both increase risk of cardiometabolic diseases. The aim is to investigate whether these factors synergistically perturb lipid metabolism in rat liver and kidney. METHODS AND RESULTS Fractional de novo lipogenesis (fDNL), intrahepatic- and intrarenal-triglycerides (IHTG and IRTG), de novo palmitate (DNPalm) content, FA composition, VLDL-TGs kinetics, and key metabolic gene expression at the end of the feeding and non-feeding phases in rats exposed to standard chow diet, chow diet + CS, 20% liquid high-fructose supplementation (HFr), or HFr+CS are measured. HFr induces hypertriglyceridemia, up-regulates fructose-metabolism and gluconeogenic enzymes, increases IHTG and DNPalm content in IHTG and IRTG, and augments fDNL at the end of the feeding phase. These changes are diminished after the non-feeding phase. CS does not exert such effects, but when combined with HFr, it reduces IHTG and visceral adiposity, enhances lipogenic gene expression and fDNL, and increases VLDL-DNPalm secretion. CONCLUSION Liquid high-fructose supplementation increases IHTG and VLDL-TG secretion after the feeding phase, the latter being the result of stimulated hepatic and renal DNL. Chronic stress potentiates the effects of high fructose on fDNL and export of newly synthesized VLDL-TGs, and decreases fructose-induced intrahepatic TG accumulation after the feeding phase.
PB  - John Wiley & Sons, Ltd
T2  - Molecular Nutrition & Food Research
T1  - Chronic Stress Potentiates High Fructose-Induced Lipogenesis in Rat Liver and Kidney.
IS  - 13
VL  - 64
DO  - 10.1002/mnfr.201901141
SP  - e1901141
ER  - 

@article{
author = "Vojnović-Milutinović, Danijela and Brkljačić, Jelena and Teofilović, Ana and Bursać, Biljana and Radovanović, Marina and Gligorovska, Ljupka and Kovačević, Sanja and Đorđević, Ana and Preitner, Frederic and Tappy, Luc and Matić, Gordana and Veličković, Nataša",
year = "2020",
abstract = "SCOPE Intake of fructose-sweetened beverages and chronic stress (CS) both increase risk of cardiometabolic diseases. The aim is to investigate whether these factors synergistically perturb lipid metabolism in rat liver and kidney. METHODS AND RESULTS Fractional de novo lipogenesis (fDNL), intrahepatic- and intrarenal-triglycerides (IHTG and IRTG), de novo palmitate (DNPalm) content, FA composition, VLDL-TGs kinetics, and key metabolic gene expression at the end of the feeding and non-feeding phases in rats exposed to standard chow diet, chow diet + CS, 20% liquid high-fructose supplementation (HFr), or HFr+CS are measured. HFr induces hypertriglyceridemia, up-regulates fructose-metabolism and gluconeogenic enzymes, increases IHTG and DNPalm content in IHTG and IRTG, and augments fDNL at the end of the feeding phase. These changes are diminished after the non-feeding phase. CS does not exert such effects, but when combined with HFr, it reduces IHTG and visceral adiposity, enhances lipogenic gene expression and fDNL, and increases VLDL-DNPalm secretion. CONCLUSION Liquid high-fructose supplementation increases IHTG and VLDL-TG secretion after the feeding phase, the latter being the result of stimulated hepatic and renal DNL. Chronic stress potentiates the effects of high fructose on fDNL and export of newly synthesized VLDL-TGs, and decreases fructose-induced intrahepatic TG accumulation after the feeding phase.",
publisher = "John Wiley & Sons, Ltd",
journal = "Molecular Nutrition & Food Research",
title = "Chronic Stress Potentiates High Fructose-Induced Lipogenesis in Rat Liver and Kidney.",
number = "13",
volume = "64",
doi = "10.1002/mnfr.201901141",
pages = "e1901141"
}

Vojnović-Milutinović, D., Brkljačić, J., Teofilović, A., Bursać, B., Radovanović, M., Gligorovska, L., Kovačević, S., Đorđević, A., Preitner, F., Tappy, L., Matić, G.,& Veličković, N.. (2020). Chronic Stress Potentiates High Fructose-Induced Lipogenesis in Rat Liver and Kidney.. in Molecular Nutrition & Food Research
John Wiley & Sons, Ltd., 64(13), e1901141.
https://doi.org/10.1002/mnfr.201901141

Vojnović-Milutinović D, Brkljačić J, Teofilović A, Bursać B, Radovanović M, Gligorovska L, Kovačević S, Đorđević A, Preitner F, Tappy L, Matić G, Veličković N. Chronic Stress Potentiates High Fructose-Induced Lipogenesis in Rat Liver and Kidney.. in Molecular Nutrition & Food Research. 2020;64(13):e1901141.
doi:10.1002/mnfr.201901141 .

Vojnović-Milutinović, Danijela, Brkljačić, Jelena, Teofilović, Ana, Bursać, Biljana, Radovanović, Marina, Gligorovska, Ljupka, Kovačević, Sanja, Đorđević, Ana, Preitner, Frederic, Tappy, Luc, Matić, Gordana, Veličković, Nataša, "Chronic Stress Potentiates High Fructose-Induced Lipogenesis in Rat Liver and Kidney." in Molecular Nutrition & Food Research, 64, no. 13 (2020):e1901141,
https://doi.org/10.1002/mnfr.201901141 . .

TY  - CONF
AU  - Veličković, Nataša
AU  - Vojnović-Milutinović, Danijela
AU  - Brkljačić, Jelena
AU  - Teofilović, Ana
AU  - Bursać, Biljana
AU  - Radovanović, Marina
AU  - Gligorovska, Ljupka
AU  - Kovačević, Sanja
AU  - Đorđević, Ana
AU  - Preitner, Frédéric
AU  - Tappy, Luc
AU  - Matić, Gordana
PY  - 2020
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4117
AB  - Overconsumption of fructoseenriched beverages and everyday stress are
both involved in the pathogenesis of metabolic disorders through their effects
on hepatic lipid metabolism. The aim of this study was to investigate
whether highfructose diet and chronic stress synergistically perturbs lipid
metabolism in rat liver. Therefore, we analyzed the effects of 9-week
20% liquid fructose diet and 4-week chronic unpredictable stress, separately
and in combination, on dyslipidemia, VLDL-TG kinetics, intrahepatic
triglycerides (IHTG), liver de novo palmitate (DNPalm) content and fatty
acid (FA) composition. In parallel, hepatic fractional de novo lipogenesis
(fDNL) by stable isotope tracer protocol, as well as expression of lipid metabolism
regulators were also analyzed. Results showed that highfructose
diet led to hypertriglyceridemia, increased plasma VLDL-TGs and free FA
(FFA), and increased visceral adiposity. Fructose diet also augmented the level of palmitate, palmitoleate and oleate in the liver, the latter being result
of increased desaturase activity. In addition, newly synthesized palmitate
(DNPalm content) was increased in the liver of fructose-fed animals,
most likely as a result of stimulated fDNL. Chronic stress alone did not
exert such effects, but when combined with fructose, stress decreased FFA
level, ameliorated fructose-induced TG accumulation, and augmented the
release of VLDL-TGs. Stress also enhanced the effects of high-fructose
diet on fDNL, which was accompanied with increased expression of key
regulators of lipid metabolism, that resulting in stimulated export of newly
synthesized palmitate in the form of VLDL-TGs. These results imply that
high-fructose diet affects hepatic lipid metabolism by stimulating fDNL
and increasing de novo synthesized palmitate, which is partially accumulated
in the liver and in part released into circulation in the form of VLDLTGs.
On the other hand, stress in combination with high-fructose diet
potentiated hepatic fDNL, but it decreased temporary TG storage and redirected
newly synthesized palmitate into VLDL-TGs. Thus, the combination
of high-fructose diet and chronic stress, as hallmarks of modern lifestyle,
exerts more detrimental influence on lipid homeostasis than the individual
factors, judged by stimulated fDNL and increased export of VLDL-TGs to
non-hepatic tissues.
PB  - European Society of Endocrinology
C3  - 22nd European Congress of Endocrinology; 2020 Sep 5-9
T1  - Fructose-induced alterations of hepatic lipid metabolism are modulated by chronic stress in male rats
DO  - 10.1530/endoabs.70.AEP435
SP  - AEP435
ER  - 

@conference{
author = "Veličković, Nataša and Vojnović-Milutinović, Danijela and Brkljačić, Jelena and Teofilović, Ana and Bursać, Biljana and Radovanović, Marina and Gligorovska, Ljupka and Kovačević, Sanja and Đorđević, Ana and Preitner, Frédéric and Tappy, Luc and Matić, Gordana",
year = "2020",
abstract = "Overconsumption of fructoseenriched beverages and everyday stress are
both involved in the pathogenesis of metabolic disorders through their effects
on hepatic lipid metabolism. The aim of this study was to investigate
whether highfructose diet and chronic stress synergistically perturbs lipid
metabolism in rat liver. Therefore, we analyzed the effects of 9-week
20% liquid fructose diet and 4-week chronic unpredictable stress, separately
and in combination, on dyslipidemia, VLDL-TG kinetics, intrahepatic
triglycerides (IHTG), liver de novo palmitate (DNPalm) content and fatty
acid (FA) composition. In parallel, hepatic fractional de novo lipogenesis
(fDNL) by stable isotope tracer protocol, as well as expression of lipid metabolism
regulators were also analyzed. Results showed that highfructose
diet led to hypertriglyceridemia, increased plasma VLDL-TGs and free FA
(FFA), and increased visceral adiposity. Fructose diet also augmented the level of palmitate, palmitoleate and oleate in the liver, the latter being result
of increased desaturase activity. In addition, newly synthesized palmitate
(DNPalm content) was increased in the liver of fructose-fed animals,
most likely as a result of stimulated fDNL. Chronic stress alone did not
exert such effects, but when combined with fructose, stress decreased FFA
level, ameliorated fructose-induced TG accumulation, and augmented the
release of VLDL-TGs. Stress also enhanced the effects of high-fructose
diet on fDNL, which was accompanied with increased expression of key
regulators of lipid metabolism, that resulting in stimulated export of newly
synthesized palmitate in the form of VLDL-TGs. These results imply that
high-fructose diet affects hepatic lipid metabolism by stimulating fDNL
and increasing de novo synthesized palmitate, which is partially accumulated
in the liver and in part released into circulation in the form of VLDLTGs.
On the other hand, stress in combination with high-fructose diet
potentiated hepatic fDNL, but it decreased temporary TG storage and redirected
newly synthesized palmitate into VLDL-TGs. Thus, the combination
of high-fructose diet and chronic stress, as hallmarks of modern lifestyle,
exerts more detrimental influence on lipid homeostasis than the individual
factors, judged by stimulated fDNL and increased export of VLDL-TGs to
non-hepatic tissues.",
publisher = "European Society of Endocrinology",
journal = "22nd European Congress of Endocrinology; 2020 Sep 5-9",
title = "Fructose-induced alterations of hepatic lipid metabolism are modulated by chronic stress in male rats",
doi = "10.1530/endoabs.70.AEP435",
pages = "AEP435"
}

Veličković, N., Vojnović-Milutinović, D., Brkljačić, J., Teofilović, A., Bursać, B., Radovanović, M., Gligorovska, L., Kovačević, S., Đorđević, A., Preitner, F., Tappy, L.,& Matić, G.. (2020). Fructose-induced alterations of hepatic lipid metabolism are modulated by chronic stress in male rats. in 22nd European Congress of Endocrinology; 2020 Sep 5-9
European Society of Endocrinology., AEP435.
https://doi.org/10.1530/endoabs.70.AEP435

Veličković N, Vojnović-Milutinović D, Brkljačić J, Teofilović A, Bursać B, Radovanović M, Gligorovska L, Kovačević S, Đorđević A, Preitner F, Tappy L, Matić G. Fructose-induced alterations of hepatic lipid metabolism are modulated by chronic stress in male rats. in 22nd European Congress of Endocrinology; 2020 Sep 5-9. 2020;:AEP435.
doi:10.1530/endoabs.70.AEP435 .

Veličković, Nataša, Vojnović-Milutinović, Danijela, Brkljačić, Jelena, Teofilović, Ana, Bursać, Biljana, Radovanović, Marina, Gligorovska, Ljupka, Kovačević, Sanja, Đorđević, Ana, Preitner, Frédéric, Tappy, Luc, Matić, Gordana, "Fructose-induced alterations of hepatic lipid metabolism are modulated by chronic stress in male rats" in 22nd European Congress of Endocrinology; 2020 Sep 5-9 (2020):AEP435,
https://doi.org/10.1530/endoabs.70.AEP435 . .

TY  - CONF
AU  - Vojnović-Milutinović, Danijela
AU  - Veličković, Nataša
AU  - Radovanović, Marina
AU  - Đorđević, Ana
AU  - Brkljačić, Jelena
AU  - Teofilović, Ana
AU  - Bursać, Biljana
AU  - Jelača, Sanja
AU  - Macut, Đuro
PY  - 2020
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4116
AB  - Polycystic ovary syndrome (PCOS) is a complex reproductive disorder that
is usually associated with metabolic disturbances such as obesity, dyslipidemia
and insulin resistance. In this study, female rats treated with nonaromatizable
5α dihydrotestosterone (DHT) were used as an animal model of
PCOS. The aim of this study was to assess the presence of inflammation in liver and visceral adipose tissue (VAT), which accompanies metabolic
disturbances in animal model of PCOS. Female (21 days old) Wistar rats
were treated subcutaneously with DHT pellets, while control animals received
placebo pellets. Glucose, triglycerides, free fatty acids (FFA) were
determined in blood plasma, while corticosterone was analyzed both in plasma
and liver. Expression of genes and proteinsinvolved in lipid metabolism,
such as sterol regulatory element binding protein1 (SREBP-1), fatty acid
synthase (FAS) and acetyl-CoA carboxylase (ACC), lipin-1, adipose tissue
triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), were analyzed
in the VAT of treated rats. Tissue inflammationevaluated by nuclear
factor kappa B (NFκB)protein level and intracellular distribution, as well as
by TNFα, IL6 and IL1β mRNA levels. Glucocorticoid signaling was examined
at the level of 11 beta hydroxysteroid dehydrogenase type 1 (11βHSD1)
and 5α-reductase, as well asby glucocorticoid receptor (GR) leveland its
subcellular distribution. The results showed that DHT treatment induced increase
of lipogenic factors (SREBP-1, lipin-1, FAS and PEPCK), while the
level of lipolytic enzyme HSL was decreasedin VAT. These molecular alterations
were accompanied by adipocyte hypertrophy, visceral obesity and
elevated plasma FFA and triglyceride concentrations. Those changes in lipid
metabolism were possible trigger for low-grade inflammation observed in
the VAT and characterized by NFκB activation and increasedIL6 and IL1β
mRNA levels. In spite of increased VAT proinflammatory mediators, the
level of proinflammatory cytokines, IL6 and IL1β, was decreased in the liver
of DHT-treated rats, while the activation of NFκB remained unchanged.
The state of suppressed inflammation in the liver could be an outcome of
stimulated glucocorticoid signaling, as judged byincreased hepatic corticosterone
level and GR activation. The augmentation of hepatic glucocorticoids
could be a net result of increased expression of 11βHSD1 and decreased
expression of 5β-reductase mRNA. In conclusion, the results showed that
abdominal obesity and dyslipidemia in the animal model of PCOS were accompanied
with hypertrophic adipocytes, lipid accumulation and low-grade
inflammation in the VAT. However, these metabolic disturbances did not resultin
hepatic inflammation due to increased tissue levels of glucocorticoids.
PB  - European Society of Endocrinology
C3  - 22nd European Congress of Endocrinology: Abstracts; 2020 Sep 5-9
T1  - Different effects of 5α-dihydrotestosterone treatment on hepatic and visceral adipose tissue inflammation in animal model of polycystic ovary syndrome
DO  - 10.1530/endoabs.70.AEP382
SP  - AEP382
ER  - 

@conference{
author = "Vojnović-Milutinović, Danijela and Veličković, Nataša and Radovanović, Marina and Đorđević, Ana and Brkljačić, Jelena and Teofilović, Ana and Bursać, Biljana and Jelača, Sanja and Macut, Đuro",
year = "2020",
abstract = "Polycystic ovary syndrome (PCOS) is a complex reproductive disorder that
is usually associated with metabolic disturbances such as obesity, dyslipidemia
and insulin resistance. In this study, female rats treated with nonaromatizable
5α dihydrotestosterone (DHT) were used as an animal model of
PCOS. The aim of this study was to assess the presence of inflammation in liver and visceral adipose tissue (VAT), which accompanies metabolic
disturbances in animal model of PCOS. Female (21 days old) Wistar rats
were treated subcutaneously with DHT pellets, while control animals received
placebo pellets. Glucose, triglycerides, free fatty acids (FFA) were
determined in blood plasma, while corticosterone was analyzed both in plasma
and liver. Expression of genes and proteinsinvolved in lipid metabolism,
such as sterol regulatory element binding protein1 (SREBP-1), fatty acid
synthase (FAS) and acetyl-CoA carboxylase (ACC), lipin-1, adipose tissue
triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), were analyzed
in the VAT of treated rats. Tissue inflammationevaluated by nuclear
factor kappa B (NFκB)protein level and intracellular distribution, as well as
by TNFα, IL6 and IL1β mRNA levels. Glucocorticoid signaling was examined
at the level of 11 beta hydroxysteroid dehydrogenase type 1 (11βHSD1)
and 5α-reductase, as well asby glucocorticoid receptor (GR) leveland its
subcellular distribution. The results showed that DHT treatment induced increase
of lipogenic factors (SREBP-1, lipin-1, FAS and PEPCK), while the
level of lipolytic enzyme HSL was decreasedin VAT. These molecular alterations
were accompanied by adipocyte hypertrophy, visceral obesity and
elevated plasma FFA and triglyceride concentrations. Those changes in lipid
metabolism were possible trigger for low-grade inflammation observed in
the VAT and characterized by NFκB activation and increasedIL6 and IL1β
mRNA levels. In spite of increased VAT proinflammatory mediators, the
level of proinflammatory cytokines, IL6 and IL1β, was decreased in the liver
of DHT-treated rats, while the activation of NFκB remained unchanged.
The state of suppressed inflammation in the liver could be an outcome of
stimulated glucocorticoid signaling, as judged byincreased hepatic corticosterone
level and GR activation. The augmentation of hepatic glucocorticoids
could be a net result of increased expression of 11βHSD1 and decreased
expression of 5β-reductase mRNA. In conclusion, the results showed that
abdominal obesity and dyslipidemia in the animal model of PCOS were accompanied
with hypertrophic adipocytes, lipid accumulation and low-grade
inflammation in the VAT. However, these metabolic disturbances did not resultin
hepatic inflammation due to increased tissue levels of glucocorticoids.",
publisher = "European Society of Endocrinology",
journal = "22nd European Congress of Endocrinology: Abstracts; 2020 Sep 5-9",
title = "Different effects of 5α-dihydrotestosterone treatment on hepatic and visceral adipose tissue inflammation in animal model of polycystic ovary syndrome",
doi = "10.1530/endoabs.70.AEP382",
pages = "AEP382"
}

Vojnović-Milutinović, D., Veličković, N., Radovanović, M., Đorđević, A., Brkljačić, J., Teofilović, A., Bursać, B., Jelača, S.,& Macut, Đ.. (2020). Different effects of 5α-dihydrotestosterone treatment on hepatic and visceral adipose tissue inflammation in animal model of polycystic ovary syndrome. in 22nd European Congress of Endocrinology: Abstracts; 2020 Sep 5-9
European Society of Endocrinology., AEP382.
https://doi.org/10.1530/endoabs.70.AEP382

Vojnović-Milutinović D, Veličković N, Radovanović M, Đorđević A, Brkljačić J, Teofilović A, Bursać B, Jelača S, Macut Đ. Different effects of 5α-dihydrotestosterone treatment on hepatic and visceral adipose tissue inflammation in animal model of polycystic ovary syndrome. in 22nd European Congress of Endocrinology: Abstracts; 2020 Sep 5-9. 2020;:AEP382.
doi:10.1530/endoabs.70.AEP382 .

Vojnović-Milutinović, Danijela, Veličković, Nataša, Radovanović, Marina, Đorđević, Ana, Brkljačić, Jelena, Teofilović, Ana, Bursać, Biljana, Jelača, Sanja, Macut, Đuro, "Different effects of 5α-dihydrotestosterone treatment on hepatic and visceral adipose tissue inflammation in animal model of polycystic ovary syndrome" in 22nd European Congress of Endocrinology: Abstracts; 2020 Sep 5-9 (2020):AEP382,
https://doi.org/10.1530/endoabs.70.AEP382 . .

TY  - JOUR
AU  - Romić, Snježana
AU  - Đorđević, Ana
AU  - Tepavčević, Snežana
AU  - Ćulafić, Tijana
AU  - Stojiljković, Mojca
AU  - Bursać, Biljana
AU  - Stanišić, Jelena
AU  - Kostić, Milan
AU  - Gligorovska, Ljupka
AU  - Korićanac, Goran
PY  - 2020
UR  - http://www.ncbi.nlm.nih.gov/pubmed/31974538
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3629
AB  - Both a diet rich in fructose and chronic stress exposure induce metabolic and cardiovascular disturbances. The aim of this study was to examine the effects of the fructose-rich diet and chronic stress, separately and in combination, on insulin signaling and molecules regulating glycogen synthesis and ion transport in the heart, and to reveal whether these effects coincide with changes in glucocorticoid receptor (GR) activation. Male Wistar rats were subjected to 10% fructose in drinking water and/or to chronic unpredictable stress for 9 weeks. Protein expression and/or phosphorylation of the insulin receptor (IR), protein tyrosine phosphatase 1B, insulin receptor substrate 1 (IRS1), protein kinase B (Akt), extracellular signal-regulated kinase 1/2 (ERK1/2), glycogen synthase kinase-3β (GSK-3β) and Na+/K+-ATPase α-subunits in cardiac tissue were analyzed by western blot. GR distribution between cytosolic and nuclear fractions was also analyzed. The fructose-rich diet decreased the level of pERK1/2 (Thr202/Tyr204) and pGSK-3β (Ser9) independently of stress, while chronic stress increased the IRS1 content and prevented the fructose diet-induced decrease of the pAkt (Ser473) level. The fructose-rich diet in combination with chronic stress reduced the protein content of cardiac IR and attenuated IRS1 upregulation. Separate treatments increased the protein content of Na+/K+-ATPase α1- and α2-subunits, while after combined treatment the α2 content was at the control level and the α1 content was lower than the control level. The effect of combined treatment on cardiac IR and α2-subunit expression could be mediated by increased GR nuclear accumulation. Our study provides new insights into the effects of chronic stress and a combination of the fructose diet and chronic stress on the studied molecules in the heart.
T2  - Food and Function
T1  - Effects of a fructose-rich diet and chronic stress on insulin signaling and regulation of glycogen synthase kinase-3 beta and the sodium-potassium pump in the hearts of male rats.
IS  - 2
VL  - 11
DO  - 10.1039/c9fo02306b
SP  - 1455
EP  - 1466
ER  - 

@article{
author = "Romić, Snježana and Đorđević, Ana and Tepavčević, Snežana and Ćulafić, Tijana and Stojiljković, Mojca and Bursać, Biljana and Stanišić, Jelena and Kostić, Milan and Gligorovska, Ljupka and Korićanac, Goran",
year = "2020",
abstract = "Both a diet rich in fructose and chronic stress exposure induce metabolic and cardiovascular disturbances. The aim of this study was to examine the effects of the fructose-rich diet and chronic stress, separately and in combination, on insulin signaling and molecules regulating glycogen synthesis and ion transport in the heart, and to reveal whether these effects coincide with changes in glucocorticoid receptor (GR) activation. Male Wistar rats were subjected to 10% fructose in drinking water and/or to chronic unpredictable stress for 9 weeks. Protein expression and/or phosphorylation of the insulin receptor (IR), protein tyrosine phosphatase 1B, insulin receptor substrate 1 (IRS1), protein kinase B (Akt), extracellular signal-regulated kinase 1/2 (ERK1/2), glycogen synthase kinase-3β (GSK-3β) and Na+/K+-ATPase α-subunits in cardiac tissue were analyzed by western blot. GR distribution between cytosolic and nuclear fractions was also analyzed. The fructose-rich diet decreased the level of pERK1/2 (Thr202/Tyr204) and pGSK-3β (Ser9) independently of stress, while chronic stress increased the IRS1 content and prevented the fructose diet-induced decrease of the pAkt (Ser473) level. The fructose-rich diet in combination with chronic stress reduced the protein content of cardiac IR and attenuated IRS1 upregulation. Separate treatments increased the protein content of Na+/K+-ATPase α1- and α2-subunits, while after combined treatment the α2 content was at the control level and the α1 content was lower than the control level. The effect of combined treatment on cardiac IR and α2-subunit expression could be mediated by increased GR nuclear accumulation. Our study provides new insights into the effects of chronic stress and a combination of the fructose diet and chronic stress on the studied molecules in the heart.",
journal = "Food and Function",
title = "Effects of a fructose-rich diet and chronic stress on insulin signaling and regulation of glycogen synthase kinase-3 beta and the sodium-potassium pump in the hearts of male rats.",
number = "2",
volume = "11",
doi = "10.1039/c9fo02306b",
pages = "1455-1466"
}

Romić, S., Đorđević, A., Tepavčević, S., Ćulafić, T., Stojiljković, M., Bursać, B., Stanišić, J., Kostić, M., Gligorovska, L.,& Korićanac, G.. (2020). Effects of a fructose-rich diet and chronic stress on insulin signaling and regulation of glycogen synthase kinase-3 beta and the sodium-potassium pump in the hearts of male rats.. in Food and Function, 11(2), 1455-1466.
https://doi.org/10.1039/c9fo02306b

Romić S, Đorđević A, Tepavčević S, Ćulafić T, Stojiljković M, Bursać B, Stanišić J, Kostić M, Gligorovska L, Korićanac G. Effects of a fructose-rich diet and chronic stress on insulin signaling and regulation of glycogen synthase kinase-3 beta and the sodium-potassium pump in the hearts of male rats.. in Food and Function. 2020;11(2):1455-1466.
doi:10.1039/c9fo02306b .

Romić, Snježana, Đorđević, Ana, Tepavčević, Snežana, Ćulafić, Tijana, Stojiljković, Mojca, Bursać, Biljana, Stanišić, Jelena, Kostić, Milan, Gligorovska, Ljupka, Korićanac, Goran, "Effects of a fructose-rich diet and chronic stress on insulin signaling and regulation of glycogen synthase kinase-3 beta and the sodium-potassium pump in the hearts of male rats." in Food and Function, 11, no. 2 (2020):1455-1466,
https://doi.org/10.1039/c9fo02306b . .

TY  - JOUR
AU  - Živanović, Jasmina
AU  - Kouroussis, Emilia
AU  - Kohl, Joshua B.
AU  - Adhikari, Bikash
AU  - Bursać, Biljana
AU  - Schott-Roux, Sonia
AU  - Petrović, Dunja
AU  - Miljković, Jan Lj.
AU  - Thomas-Lopez, Daniel
AU  - Jung, Youngeun
AU  - Miler, Marko
AU  - Mitchell, Sarah
AU  - Milošević, Verica
AU  - Gomes, Jose Eduardo
AU  - Benhar, Moran
AU  - Gonzales-Zorn, Bruno
AU  - Ivanović-Burmazović, Ivana
AU  - Torregrossa, Roberta
AU  - Mitchell, James R.
AU  - Whiteman, Matthew
AU  - Schwarz, Guenter
AU  - Snyder, Solomon H.
AU  - Paul, Bindu D.
AU  - Carroll, Kate S.
AU  - Filipović, Miloš R.
PY  - 2019
UR  - https://www.sciencedirect.com/science/article/abs/pii/S1550413119305625
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3518
AB  - Life on Earth emerged in a hydrogen sulfide (H2S)-rich environment eons ago and with it protein persulfidation mediated by H2S evolved as a signaling mechanism. Protein persulfidation (S-sulfhydration) is a post-translational modification of reactive cysteine residues, which modulate protein structure and/or function. Persulfides are difficult to label and study due to their reactivity and similarity with cysteine. Here, we report a facile strategy for chemoselective persulfide bioconjugation using dimedone-based probes, to achieve highly selective, rapid, and robust persulfide labeling in biological samples with broad utility. Using this method, we show persulfidation is an evolutionarily conserved modification and waves of persulfidation are employed by cells to resolve sulfenylation and prevent irreversible cysteine overoxidation preserving protein function. We report an age-associated decline in persulfidation that is conserved across evolutionary boundaries. Accordingly, dietary or pharmacological interventions to increase persulfidation associate with increased longevity and improved capacity to cope with stress stimuli.
T2  - Cell Metabolism
T1  - Selective Persulfide Detection Reveals Evolutionarily Conserved Antiaging Effects of S-Sulfhydration
IS  - 6
VL  - 30
DO  - 10.1016/J.CMET.2019.10.007
SP  - 1152
EP  - 1170.e13
ER  - 

@article{
author = "Živanović, Jasmina and Kouroussis, Emilia and Kohl, Joshua B. and Adhikari, Bikash and Bursać, Biljana and Schott-Roux, Sonia and Petrović, Dunja and Miljković, Jan Lj. and Thomas-Lopez, Daniel and Jung, Youngeun and Miler, Marko and Mitchell, Sarah and Milošević, Verica and Gomes, Jose Eduardo and Benhar, Moran and Gonzales-Zorn, Bruno and Ivanović-Burmazović, Ivana and Torregrossa, Roberta and Mitchell, James R. and Whiteman, Matthew and Schwarz, Guenter and Snyder, Solomon H. and Paul, Bindu D. and Carroll, Kate S. and Filipović, Miloš R.",
year = "2019",
abstract = "Life on Earth emerged in a hydrogen sulfide (H2S)-rich environment eons ago and with it protein persulfidation mediated by H2S evolved as a signaling mechanism. Protein persulfidation (S-sulfhydration) is a post-translational modification of reactive cysteine residues, which modulate protein structure and/or function. Persulfides are difficult to label and study due to their reactivity and similarity with cysteine. Here, we report a facile strategy for chemoselective persulfide bioconjugation using dimedone-based probes, to achieve highly selective, rapid, and robust persulfide labeling in biological samples with broad utility. Using this method, we show persulfidation is an evolutionarily conserved modification and waves of persulfidation are employed by cells to resolve sulfenylation and prevent irreversible cysteine overoxidation preserving protein function. We report an age-associated decline in persulfidation that is conserved across evolutionary boundaries. Accordingly, dietary or pharmacological interventions to increase persulfidation associate with increased longevity and improved capacity to cope with stress stimuli.",
journal = "Cell Metabolism",
title = "Selective Persulfide Detection Reveals Evolutionarily Conserved Antiaging Effects of S-Sulfhydration",
number = "6",
volume = "30",
doi = "10.1016/J.CMET.2019.10.007",
pages = "1152-1170.e13"
}

Živanović, J., Kouroussis, E., Kohl, J. B., Adhikari, B., Bursać, B., Schott-Roux, S., Petrović, D., Miljković, J. Lj., Thomas-Lopez, D., Jung, Y., Miler, M., Mitchell, S., Milošević, V., Gomes, J. E., Benhar, M., Gonzales-Zorn, B., Ivanović-Burmazović, I., Torregrossa, R., Mitchell, J. R., Whiteman, M., Schwarz, G., Snyder, S. H., Paul, B. D., Carroll, K. S.,& Filipović, M. R.. (2019). Selective Persulfide Detection Reveals Evolutionarily Conserved Antiaging Effects of S-Sulfhydration. in Cell Metabolism, 30(6), 1152-1170.e13.
https://doi.org/10.1016/J.CMET.2019.10.007

Živanović J, Kouroussis E, Kohl JB, Adhikari B, Bursać B, Schott-Roux S, Petrović D, Miljković JL, Thomas-Lopez D, Jung Y, Miler M, Mitchell S, Milošević V, Gomes JE, Benhar M, Gonzales-Zorn B, Ivanović-Burmazović I, Torregrossa R, Mitchell JR, Whiteman M, Schwarz G, Snyder SH, Paul BD, Carroll KS, Filipović MR. Selective Persulfide Detection Reveals Evolutionarily Conserved Antiaging Effects of S-Sulfhydration. in Cell Metabolism. 2019;30(6):1152-1170.e13.
doi:10.1016/J.CMET.2019.10.007 .

Živanović, Jasmina, Kouroussis, Emilia, Kohl, Joshua B., Adhikari, Bikash, Bursać, Biljana, Schott-Roux, Sonia, Petrović, Dunja, Miljković, Jan Lj., Thomas-Lopez, Daniel, Jung, Youngeun, Miler, Marko, Mitchell, Sarah, Milošević, Verica, Gomes, Jose Eduardo, Benhar, Moran, Gonzales-Zorn, Bruno, Ivanović-Burmazović, Ivana, Torregrossa, Roberta, Mitchell, James R., Whiteman, Matthew, Schwarz, Guenter, Snyder, Solomon H., Paul, Bindu D., Carroll, Kate S., Filipović, Miloš R., "Selective Persulfide Detection Reveals Evolutionarily Conserved Antiaging Effects of S-Sulfhydration" in Cell Metabolism, 30, no. 6 (2019):1152-1170.e13,
https://doi.org/10.1016/J.CMET.2019.10.007 . .

TY  - CONF
AU  - Veličković, Nataša
AU  - Vojnović-Milutinović, Danijela
AU  - Brkljačić, Jelena
AU  - Teofilović, Ana
AU  - Bursać, Biljana
AU  - Radovanović, Marina
AU  - Gligorovska, Ljupka
AU  - Kovačević, Sanja
AU  - Matić, Gordana
AU  - Đorđević, Ana
PY  - 2019
UR  - https://www.isos.rs/congress-2019
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3991
AB  - Fructose overconsumption, especially in the form of sweetened beverages, has been linked to development of obesity, insulin resistance, dyslipidemia and type 2 diabetes. In rodents, high-fructose diet leads to hypertriglyceridemia, ectopic fat deposition and insulin resistance. Metabolically triggered inflammation (metaflammation) is now recognized as a link between nutrient signals and insulin resistance and considered as usual suspect for metabolic disturbances. Metaflammation usually evolve from visceral adipose tissue, progresses to liver and brain strucures, and results in peripheral insulin resistance, lipid accumulation and oxidative stress. Hence, the aim of our study was to investigate metaflammation as a trigger for fructose-induced metabolic disturbances. Experiments were performed on male Wistar rats fed with different concentrations of liquid fructose (10, 20 and 60%) during 9 weeks. Physiological and biochemical parameters, hepatic and brain inflammation, indicators of peripheral and systemic insulin resistance, as well as hepatic lipogenesis and oxidative stress were examined. The results demonstrated that fructose-enriched diet generally led to increased proinflamatory cytokines in the liver, hippocampus and hypothalamus, and to stimulated activation of proinflamatory kinases NFκB and JNK, while it did not change the expression of inflammasome component NLRP3, toll-like receptor 4 or anti-inflammatory cytokines in the liver. The observed metabolic inflammation was accompanied with impaired glucose tolerance after 10 and 20% fructose-enriched diet, while decreased hepatic insulin sensitivity, hypetriglyceridemia and increased expression of hepatic lipogenic genes were observed after all fructose diets. The treatment of fructose-fed rats with chronic unpredictable stress annulled the effects of fructose on hepatic and hypothalamic inflammation and glucose tolerance, but did not alter fructose-induced effects on lipogenesis and insulin signaling. The results suggest that fructose-induced metaflammation and systemic insulin resistance are closely interconnected, while the link between inflammation and other metabolic disturbances could still be a matter of debate.
PB  - Institute for Biological Research "Siniša Stanković" - National Institute of Republic of Serbia, University of Belgrade
PB  - Immunological Society of Serbia
C3  - Immunology at the Confluence of Multidisciplinary Approaches : abstract book
T1  - Is Metaflammation a Usual Suspect for Fructose-induced Metabolic Disturbances?
SP  - 51
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_3991
ER  - 

@conference{
author = "Veličković, Nataša and Vojnović-Milutinović, Danijela and Brkljačić, Jelena and Teofilović, Ana and Bursać, Biljana and Radovanović, Marina and Gligorovska, Ljupka and Kovačević, Sanja and Matić, Gordana and Đorđević, Ana",
year = "2019",
abstract = "Fructose overconsumption, especially in the form of sweetened beverages, has been linked to development of obesity, insulin resistance, dyslipidemia and type 2 diabetes. In rodents, high-fructose diet leads to hypertriglyceridemia, ectopic fat deposition and insulin resistance. Metabolically triggered inflammation (metaflammation) is now recognized as a link between nutrient signals and insulin resistance and considered as usual suspect for metabolic disturbances. Metaflammation usually evolve from visceral adipose tissue, progresses to liver and brain strucures, and results in peripheral insulin resistance, lipid accumulation and oxidative stress. Hence, the aim of our study was to investigate metaflammation as a trigger for fructose-induced metabolic disturbances. Experiments were performed on male Wistar rats fed with different concentrations of liquid fructose (10, 20 and 60%) during 9 weeks. Physiological and biochemical parameters, hepatic and brain inflammation, indicators of peripheral and systemic insulin resistance, as well as hepatic lipogenesis and oxidative stress were examined. The results demonstrated that fructose-enriched diet generally led to increased proinflamatory cytokines in the liver, hippocampus and hypothalamus, and to stimulated activation of proinflamatory kinases NFκB and JNK, while it did not change the expression of inflammasome component NLRP3, toll-like receptor 4 or anti-inflammatory cytokines in the liver. The observed metabolic inflammation was accompanied with impaired glucose tolerance after 10 and 20% fructose-enriched diet, while decreased hepatic insulin sensitivity, hypetriglyceridemia and increased expression of hepatic lipogenic genes were observed after all fructose diets. The treatment of fructose-fed rats with chronic unpredictable stress annulled the effects of fructose on hepatic and hypothalamic inflammation and glucose tolerance, but did not alter fructose-induced effects on lipogenesis and insulin signaling. The results suggest that fructose-induced metaflammation and systemic insulin resistance are closely interconnected, while the link between inflammation and other metabolic disturbances could still be a matter of debate.",
publisher = "Institute for Biological Research "Siniša Stanković" - National Institute of Republic of Serbia, University of Belgrade, Immunological Society of Serbia",
journal = "Immunology at the Confluence of Multidisciplinary Approaches : abstract book",
title = "Is Metaflammation a Usual Suspect for Fructose-induced Metabolic Disturbances?",
pages = "51",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_3991"
}

Veličković, N., Vojnović-Milutinović, D., Brkljačić, J., Teofilović, A., Bursać, B., Radovanović, M., Gligorovska, L., Kovačević, S., Matić, G.,& Đorđević, A.. (2019). Is Metaflammation a Usual Suspect for Fructose-induced Metabolic Disturbances?. in Immunology at the Confluence of Multidisciplinary Approaches : abstract book
Institute for Biological Research "Siniša Stanković" - National Institute of Republic of Serbia, University of Belgrade., 51.
https://hdl.handle.net/21.15107/rcub_ibiss_3991

Veličković N, Vojnović-Milutinović D, Brkljačić J, Teofilović A, Bursać B, Radovanović M, Gligorovska L, Kovačević S, Matić G, Đorđević A. Is Metaflammation a Usual Suspect for Fructose-induced Metabolic Disturbances?. in Immunology at the Confluence of Multidisciplinary Approaches : abstract book. 2019;:51.
https://hdl.handle.net/21.15107/rcub_ibiss_3991 .

Veličković, Nataša, Vojnović-Milutinović, Danijela, Brkljačić, Jelena, Teofilović, Ana, Bursać, Biljana, Radovanović, Marina, Gligorovska, Ljupka, Kovačević, Sanja, Matić, Gordana, Đorđević, Ana, "Is Metaflammation a Usual Suspect for Fructose-induced Metabolic Disturbances?" in Immunology at the Confluence of Multidisciplinary Approaches : abstract book (2019):51,
https://hdl.handle.net/21.15107/rcub_ibiss_3991 .

TY  - CONF
AU  - Đorđević, Ana
AU  - Vujković Cvijin, Ivan I.
AU  - Lešović, Snežana J.
AU  - Gligorovska, Ljupka
AU  - Bursać, Biljana
AU  - Vojnović-Milutinović, Danijela
AU  - Matić, Gordana
PY  - 2019
UR  - https://blog.u-bourgogne.fr/cost-nutredox/wp-content/uploads/sites/81/2019/09/20191002-Lisbon-Abstract-book-vf-min.pdf
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3994
AB  - Prevalence  of  obesity  among  adolescents  has  been  constantly  increasing  in  the  last decades. The  treatment  of  obesity  requires  multidisciplinary  approach,  which  includes dietary management. However, not all people respond to dietary intervention in the same way. Since gut microbiota has been tightly linked to obesity, the aim of this pilot study was to assess whether microbiota composition affects the outcome of the hypocaloric diet on weight loss in obese male adolescents.Forty-four obese male adolescents(average BMI>95thpercentile), 12-15 years old, were selected  from  the  large  cohort  of  500  patients.  Their  body  composition  was  assessed before  and  after  3-week  balanced  hypocaloric  diet  (1200-1700  kcal)  with  preserved nutritional  value.    Microbial  DNA  was  extracted  from  cryopreserved  fecal  samples collected before the dietary intervention. Alterations of the gut microbiota were analyzed using MiSeq 16S rRNA gene sequencing. The primary outcome of the diet was the change in body weight and BMI. Subjects were divided  in  2  groups  according  to  significant  differences  in  delta  BMI  after  the  dietary intervention (P< 0.001). The values for delta BMIs were 1.93 and 2.66 for groups 1 and 2,  respectively.  The  observed  differences  were  associated  with  fecal  microbiome composition.  Group  2  subjects,  which  have  lost  more  weight,  originally  had  less Firmicutes   spp. bacteria,   more   specifically   from   families Lachnospiraceae and Desulfovibrionaceae. These  preliminary  results  show  that  the  ability  for  diet-induced  weight  loss  could  be associated   with   microbiota   composition.   Whether   certain   bacterial   taxa   represent facilitating or  resilience  factor  for  weight  loss  is  yet  to  be  determined  in  future experiments.
PB  - COST (European Cooperation in Science and Technology), NutRedox COST Action CA 16112
PB  - Universidade Lusófona
C3  - Lisbon, Portugal: NutRedox COST (European Cooperation in Science and Technology) Action CA 16112 Abstract Book
T1  - Gut Microbiota Composition Influences the Extent of Weight Loss After Hypocaloric Diet in Obese Male Adolescents
SP  - 36
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_3994
ER  - 

@conference{
author = "Đorđević, Ana and Vujković Cvijin, Ivan I. and Lešović, Snežana J. and Gligorovska, Ljupka and Bursać, Biljana and Vojnović-Milutinović, Danijela and Matić, Gordana",
year = "2019",
abstract = "Prevalence  of  obesity  among  adolescents  has  been  constantly  increasing  in  the  last decades. The  treatment  of  obesity  requires  multidisciplinary  approach,  which  includes dietary management. However, not all people respond to dietary intervention in the same way. Since gut microbiota has been tightly linked to obesity, the aim of this pilot study was to assess whether microbiota composition affects the outcome of the hypocaloric diet on weight loss in obese male adolescents.Forty-four obese male adolescents(average BMI>95thpercentile), 12-15 years old, were selected  from  the  large  cohort  of  500  patients.  Their  body  composition  was  assessed before  and  after  3-week  balanced  hypocaloric  diet  (1200-1700  kcal)  with  preserved nutritional  value.    Microbial  DNA  was  extracted  from  cryopreserved  fecal  samples collected before the dietary intervention. Alterations of the gut microbiota were analyzed using MiSeq 16S rRNA gene sequencing. The primary outcome of the diet was the change in body weight and BMI. Subjects were divided  in  2  groups  according  to  significant  differences  in  delta  BMI  after  the  dietary intervention (P< 0.001). The values for delta BMIs were 1.93 and 2.66 for groups 1 and 2,  respectively.  The  observed  differences  were  associated  with  fecal  microbiome composition.  Group  2  subjects,  which  have  lost  more  weight,  originally  had  less Firmicutes   spp. bacteria,   more   specifically   from   families Lachnospiraceae and Desulfovibrionaceae. These  preliminary  results  show  that  the  ability  for  diet-induced  weight  loss  could  be associated   with   microbiota   composition.   Whether   certain   bacterial   taxa   represent facilitating or  resilience  factor  for  weight  loss  is  yet  to  be  determined  in  future experiments.",
publisher = "COST (European Cooperation in Science and Technology), NutRedox COST Action CA 16112, Universidade Lusófona",
journal = "Lisbon, Portugal: NutRedox COST (European Cooperation in Science and Technology) Action CA 16112 Abstract Book",
title = "Gut Microbiota Composition Influences the Extent of Weight Loss After Hypocaloric Diet in Obese Male Adolescents",
pages = "36",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_3994"
}

Đorđević, A., Vujković Cvijin, I. I., Lešović, S. J., Gligorovska, L., Bursać, B., Vojnović-Milutinović, D.,& Matić, G.. (2019). Gut Microbiota Composition Influences the Extent of Weight Loss After Hypocaloric Diet in Obese Male Adolescents. in Lisbon, Portugal: NutRedox COST (European Cooperation in Science and Technology) Action CA 16112 Abstract Book
COST (European Cooperation in Science and Technology), NutRedox COST Action CA 16112., 36.
https://hdl.handle.net/21.15107/rcub_ibiss_3994

Đorđević A, Vujković Cvijin II, Lešović SJ, Gligorovska L, Bursać B, Vojnović-Milutinović D, Matić G. Gut Microbiota Composition Influences the Extent of Weight Loss After Hypocaloric Diet in Obese Male Adolescents. in Lisbon, Portugal: NutRedox COST (European Cooperation in Science and Technology) Action CA 16112 Abstract Book. 2019;:36.
https://hdl.handle.net/21.15107/rcub_ibiss_3994 .

Đorđević, Ana, Vujković Cvijin, Ivan I., Lešović, Snežana J., Gligorovska, Ljupka, Bursać, Biljana, Vojnović-Milutinović, Danijela, Matić, Gordana, "Gut Microbiota Composition Influences the Extent of Weight Loss After Hypocaloric Diet in Obese Male Adolescents" in Lisbon, Portugal: NutRedox COST (European Cooperation in Science and Technology) Action CA 16112 Abstract Book (2019):36,
https://hdl.handle.net/21.15107/rcub_ibiss_3994 .

TY  - CONF
AU  - Kovačević, Sanja
AU  - Bursać, Biljana
AU  - Đorđević, Ana
AU  - Gligorovska, Ljupka
AU  - Matić, Gordana
AU  - Elaković, Ivana
PY  - 2019
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3988
AB  - Background: Increased consumption of caloric food rich in fructose and daily exposure to unpredictable stress became hallmarks of modern lifestyle and have been associated with the development of metabolic syndrome, type2 diabetes and cardiovascular diseases1,2. Visceral  adipose  tissue  (VAT)  and  muscles are important centers of lipid and glucose metabolism and metabolic disturbances  in  these  organs  and  their crosstalk  could  vastly contribute to the development of metabolic diseases3,4. The  aim: To  elucidate  whether prolonged combination of fructose  over consumption and chronic stress disturbs lipid metabolism and insulin signaling in rat VAT and muscle. Methods: We  examined the  effects  of  9-week  fructose-enriched diet with  and  without exposure to unpredictable stress on expression of genes and level of proteins involved in lipid  uptake (lipoprotein lipase, fatty  acid  translocase  and fatty  acid transport  protein), de novo lipogenesis    (acetyl-CoA    carboxylase    and fatty    acid    synthase), lipolysis (hormone sensitive lipase and adipose   triglyceride   lipase)   and fatty   acids oxidation (carnitine  palmitoyltransferase  I)  in VAT  and muscle of  male  Wistar  rats.  Additionally, muscle  insulin  signaling  was  analyzed at the  level  of insulin receptor  substrate-1  (IRS1) and Akt kinase, and their activating and inhibitory phosphorylations. Results: Combination  of  fructose  overconsumption  and  stress increased plasma insulin and free fatty acids level, upregulated expression of both lipolytic and lipogenic genes in VAT and stimulated lipid uptake, lipolysis and β-oxidation in muscle. Furthermore, reduced protein  content  and  stimulatory  phosphorylation  of IRS1  and Akt  kinase, together  with unchanged inhibitory phosphorylation of IRS1 was observed in muscle. Conclusions: The  results show that the  combination  of fructose  over consumption and chronic stress disturbs lipid metabolism in VAT and muscle. Importantly, upregulated VAT lipolysis  elevates  plasma  free  fatty  acids, which  intensify their  influx  to  muscles  possibly leading to muscle insulin resistance detected in fructose fed stressed rats.
PB  - EMBO Press
C3  - EMBO Workshop Organ crosstalk in energy balance and metabolic disease; 2019 Apr 8-11; Sancti Petri, Chiclana, Cádiz, Spain
T1  - Combination Of Fructose And Stress Induces Insulin Resistance And Disturbs Lipid Metabolism In Muscle And Adipose Tissue Of Rats
SP  - 45
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_3988
ER  - 

@conference{
author = "Kovačević, Sanja and Bursać, Biljana and Đorđević, Ana and Gligorovska, Ljupka and Matić, Gordana and Elaković, Ivana",
year = "2019",
abstract = "Background: Increased consumption of caloric food rich in fructose and daily exposure to unpredictable stress became hallmarks of modern lifestyle and have been associated with the development of metabolic syndrome, type2 diabetes and cardiovascular diseases1,2. Visceral  adipose  tissue  (VAT)  and  muscles are important centers of lipid and glucose metabolism and metabolic disturbances  in  these  organs  and  their crosstalk  could  vastly contribute to the development of metabolic diseases3,4. The  aim: To  elucidate  whether prolonged combination of fructose  over consumption and chronic stress disturbs lipid metabolism and insulin signaling in rat VAT and muscle. Methods: We  examined the  effects  of  9-week  fructose-enriched diet with  and  without exposure to unpredictable stress on expression of genes and level of proteins involved in lipid  uptake (lipoprotein lipase, fatty  acid  translocase  and fatty  acid transport  protein), de novo lipogenesis    (acetyl-CoA    carboxylase    and fatty    acid    synthase), lipolysis (hormone sensitive lipase and adipose   triglyceride   lipase)   and fatty   acids oxidation (carnitine  palmitoyltransferase  I)  in VAT  and muscle of  male  Wistar  rats.  Additionally, muscle  insulin  signaling  was  analyzed at the  level  of insulin receptor  substrate-1  (IRS1) and Akt kinase, and their activating and inhibitory phosphorylations. Results: Combination  of  fructose  overconsumption  and  stress increased plasma insulin and free fatty acids level, upregulated expression of both lipolytic and lipogenic genes in VAT and stimulated lipid uptake, lipolysis and β-oxidation in muscle. Furthermore, reduced protein  content  and  stimulatory  phosphorylation  of IRS1  and Akt  kinase, together  with unchanged inhibitory phosphorylation of IRS1 was observed in muscle. Conclusions: The  results show that the  combination  of fructose  over consumption and chronic stress disturbs lipid metabolism in VAT and muscle. Importantly, upregulated VAT lipolysis  elevates  plasma  free  fatty  acids, which  intensify their  influx  to  muscles  possibly leading to muscle insulin resistance detected in fructose fed stressed rats.",
publisher = "EMBO Press",
journal = "EMBO Workshop Organ crosstalk in energy balance and metabolic disease; 2019 Apr 8-11; Sancti Petri, Chiclana, Cádiz, Spain",
title = "Combination Of Fructose And Stress Induces Insulin Resistance And Disturbs Lipid Metabolism In Muscle And Adipose Tissue Of Rats",
pages = "45",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_3988"
}

Kovačević, S., Bursać, B., Đorđević, A., Gligorovska, L., Matić, G.,& Elaković, I.. (2019). Combination Of Fructose And Stress Induces Insulin Resistance And Disturbs Lipid Metabolism In Muscle And Adipose Tissue Of Rats. in EMBO Workshop Organ crosstalk in energy balance and metabolic disease; 2019 Apr 8-11; Sancti Petri, Chiclana, Cádiz, Spain
EMBO Press., 45.
https://hdl.handle.net/21.15107/rcub_ibiss_3988

Kovačević S, Bursać B, Đorđević A, Gligorovska L, Matić G, Elaković I. Combination Of Fructose And Stress Induces Insulin Resistance And Disturbs Lipid Metabolism In Muscle And Adipose Tissue Of Rats. in EMBO Workshop Organ crosstalk in energy balance and metabolic disease; 2019 Apr 8-11; Sancti Petri, Chiclana, Cádiz, Spain. 2019;:45.
https://hdl.handle.net/21.15107/rcub_ibiss_3988 .

Kovačević, Sanja, Bursać, Biljana, Đorđević, Ana, Gligorovska, Ljupka, Matić, Gordana, Elaković, Ivana, "Combination Of Fructose And Stress Induces Insulin Resistance And Disturbs Lipid Metabolism In Muscle And Adipose Tissue Of Rats" in EMBO Workshop Organ crosstalk in energy balance and metabolic disease; 2019 Apr 8-11; Sancti Petri, Chiclana, Cádiz, Spain (2019):45,
https://hdl.handle.net/21.15107/rcub_ibiss_3988 .

TY  - JOUR
AU  - Andrejević, Marko
AU  - Keckarević Marković, Milica
AU  - Bursać, Biljana
AU  - Mihajlović, Milica
AU  - Tanasić, Vanja
AU  - Kecmanović, Miljana
AU  - Keckarevic, Dušan
PY  - 2019
UR  - http://link.springer.com/10.1007/s12024-019-00096-4
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3289
AB  - Mitochondrial DNA (mtDNA), especially the gene for cytochrome b (MT-CYB), has been found to be highly informative for species identification. In this study, we present the results of the analysis of a 127 bp long fragment of MT-CYB, amplified using universal primers, variable enough to be used for species identification and discrimination, even in highly degraded animal samples. The total number of analyzed species in this study was 30, including 17 mammalian and 13 bird species. Using a newly created primer pair, we successfully amplified and sequenced the target sequence in almost all tested species. The amplification was incomplete in just two species, and as a result, partial, but still variable sequences, were obtained. Using the target fragment we successfully identified all tested samples. Initial results suggested that the intraspecies genetic diversity of the target region, in all tested species, was low - from 0 to 4.72%. The interspecies genetic diversity of the target region, crucial for successful discrimination, showed relatively high diversity, ranging from 8.36% to 42.52%. Given its short length, the target region should be used for species determination, particularly in samples that are degraded or are low in DNA quantity.
T2  - Forensic Science, Medicine, and Pathology
T1  - Identification of a broad spectrum of mammalian and avian species using the short fragment of the mitochondrially encoded cytochrome b gene.
DO  - 10.1007/s12024-019-00096-4
ER  - 

@article{
author = "Andrejević, Marko and Keckarević Marković, Milica and Bursać, Biljana and Mihajlović, Milica and Tanasić, Vanja and Kecmanović, Miljana and Keckarevic, Dušan",
year = "2019",
abstract = "Mitochondrial DNA (mtDNA), especially the gene for cytochrome b (MT-CYB), has been found to be highly informative for species identification. In this study, we present the results of the analysis of a 127 bp long fragment of MT-CYB, amplified using universal primers, variable enough to be used for species identification and discrimination, even in highly degraded animal samples. The total number of analyzed species in this study was 30, including 17 mammalian and 13 bird species. Using a newly created primer pair, we successfully amplified and sequenced the target sequence in almost all tested species. The amplification was incomplete in just two species, and as a result, partial, but still variable sequences, were obtained. Using the target fragment we successfully identified all tested samples. Initial results suggested that the intraspecies genetic diversity of the target region, in all tested species, was low - from 0 to 4.72%. The interspecies genetic diversity of the target region, crucial for successful discrimination, showed relatively high diversity, ranging from 8.36% to 42.52%. Given its short length, the target region should be used for species determination, particularly in samples that are degraded or are low in DNA quantity.",
journal = "Forensic Science, Medicine, and Pathology",
title = "Identification of a broad spectrum of mammalian and avian species using the short fragment of the mitochondrially encoded cytochrome b gene.",
doi = "10.1007/s12024-019-00096-4"
}

Andrejević, M., Keckarević Marković, M., Bursać, B., Mihajlović, M., Tanasić, V., Kecmanović, M.,& Keckarevic, D.. (2019). Identification of a broad spectrum of mammalian and avian species using the short fragment of the mitochondrially encoded cytochrome b gene.. in Forensic Science, Medicine, and Pathology.
https://doi.org/10.1007/s12024-019-00096-4

Andrejević M, Keckarević Marković M, Bursać B, Mihajlović M, Tanasić V, Kecmanović M, Keckarevic D. Identification of a broad spectrum of mammalian and avian species using the short fragment of the mitochondrially encoded cytochrome b gene.. in Forensic Science, Medicine, and Pathology. 2019;.
doi:10.1007/s12024-019-00096-4 .

Andrejević, Marko, Keckarević Marković, Milica, Bursać, Biljana, Mihajlović, Milica, Tanasić, Vanja, Kecmanović, Miljana, Keckarevic, Dušan, "Identification of a broad spectrum of mammalian and avian species using the short fragment of the mitochondrially encoded cytochrome b gene." in Forensic Science, Medicine, and Pathology (2019),
https://doi.org/10.1007/s12024-019-00096-4 . .

TY  - JOUR
AU  - Gligorovska, Ljupka
AU  - Bursać, Biljana
AU  - Kovačević, Sanja
AU  - Veličković, Nataša
AU  - Matić, Gordana
AU  - Đorđević, Ana
PY  - 2019
UR  - https://joe.bioscientifica.com/view/journals/joe/240/2/JOE-18-0333.xml
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3243
AB  - The macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine involved in inflammation, regulation of energy metabolism and glucocorticoid action. Chronic low-grade inflammation may be caused by fructose intake, contributing to visceral adipose tissue (VAT) dysfunction. Since MIF is a known antagonist of glucocorticoid signaling, and deregulated glucocorticoid signaling can contribute to lipid metabolism disturbances, we hypothesized that altered MIF signaling might underlie fructose-induced adiposity through glucocorticoid action. We analyzed physiological and biochemical parameters, adipose tissue histology, insulin sensitivity and lipid metabolism in wild type and MIF-/- C57Bl/6J mice consuming 20% fructose solution for 9 weeks. Glucocorticoid prereceptor metabolism and glucocorticoid receptor (GR) protein level were examined in VAT, together with the expression of glucocorticoid-target genes involved in lipid metabolism. The expression of adipogenic and lipogenic transcriptional regulators peroxisome proliferator activated receptor gamma (PPARG) and sterol regulatory element-binding protein 1c (SREBP1c) was also assessed. Results showed disturbed insulin sensitivity in all MIF-/- mice, regardless of the diet. Mice on fructose diet had increased energy intake, but increased visceral adiposity and enlarged adipocytes were observed only in fructose-fed MIF-/- mice. Increased VAT corticosterone level and 11 beta-hydroxysteroid dehydrogenase type 1, hexose-6-phosphate dehydrogenase and GR protein levels were observed in the same animals, together with induced expression of examined lipogenic genes and accumulation of PPARG and SREBP1c. In conclusion, the results showed that dietary fructose was associated with increased visceral adiposity through activation of GR-regulated lipogenic genes, but only in the absence of MIF, which set the state of hyperinsulinemia and insulin resistance.
T2  - Journal of Endocrinology
T1  - Mif deficiency promotes adiposity in fructose-fed mice.
DO  - 10.1530/JOE-18-0333
ER  - 

@article{
author = "Gligorovska, Ljupka and Bursać, Biljana and Kovačević, Sanja and Veličković, Nataša and Matić, Gordana and Đorđević, Ana",
year = "2019",
abstract = "The macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine involved in inflammation, regulation of energy metabolism and glucocorticoid action. Chronic low-grade inflammation may be caused by fructose intake, contributing to visceral adipose tissue (VAT) dysfunction. Since MIF is a known antagonist of glucocorticoid signaling, and deregulated glucocorticoid signaling can contribute to lipid metabolism disturbances, we hypothesized that altered MIF signaling might underlie fructose-induced adiposity through glucocorticoid action. We analyzed physiological and biochemical parameters, adipose tissue histology, insulin sensitivity and lipid metabolism in wild type and MIF-/- C57Bl/6J mice consuming 20% fructose solution for 9 weeks. Glucocorticoid prereceptor metabolism and glucocorticoid receptor (GR) protein level were examined in VAT, together with the expression of glucocorticoid-target genes involved in lipid metabolism. The expression of adipogenic and lipogenic transcriptional regulators peroxisome proliferator activated receptor gamma (PPARG) and sterol regulatory element-binding protein 1c (SREBP1c) was also assessed. Results showed disturbed insulin sensitivity in all MIF-/- mice, regardless of the diet. Mice on fructose diet had increased energy intake, but increased visceral adiposity and enlarged adipocytes were observed only in fructose-fed MIF-/- mice. Increased VAT corticosterone level and 11 beta-hydroxysteroid dehydrogenase type 1, hexose-6-phosphate dehydrogenase and GR protein levels were observed in the same animals, together with induced expression of examined lipogenic genes and accumulation of PPARG and SREBP1c. In conclusion, the results showed that dietary fructose was associated with increased visceral adiposity through activation of GR-regulated lipogenic genes, but only in the absence of MIF, which set the state of hyperinsulinemia and insulin resistance.",
journal = "Journal of Endocrinology",
title = "Mif deficiency promotes adiposity in fructose-fed mice.",
doi = "10.1530/JOE-18-0333"
}

Gligorovska, L., Bursać, B., Kovačević, S., Veličković, N., Matić, G.,& Đorđević, A.. (2019). Mif deficiency promotes adiposity in fructose-fed mice.. in Journal of Endocrinology.
https://doi.org/10.1530/JOE-18-0333

Gligorovska L, Bursać B, Kovačević S, Veličković N, Matić G, Đorđević A. Mif deficiency promotes adiposity in fructose-fed mice.. in Journal of Endocrinology. 2019;.
doi:10.1530/JOE-18-0333 .

Gligorovska, Ljupka, Bursać, Biljana, Kovačević, Sanja, Veličković, Nataša, Matić, Gordana, Đorđević, Ana, "Mif deficiency promotes adiposity in fructose-fed mice." in Journal of Endocrinology (2019),
https://doi.org/10.1530/JOE-18-0333 . .

TY  - JOUR
AU  - Gligorovska, Ljupka
AU  - Bursać, Biljana
AU  - Kovačević, Sanja
AU  - Veličković, Nataša
AU  - Matić, Gordana
AU  - Đorđević, Ana
PY  - 2019
UR  - https://joe.bioscientifica.com/view/journals/joe/240/2/JOE-18-0333.xml
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3240
AB  - The macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine involved in inflammation, regulation of energy metabolism and glucocorticoid action. Chronic low-grade inflammation may be caused by fructose intake, contributing to visceral adipose tissue (VAT) dysfunction. Since MIF is a known antagonist of glucocorticoid signaling, and deregulated glucocorticoid signaling can contribute to lipid metabolism disturbances, we hypothesized that altered MIF signaling might underlie fructose-induced adiposity through glucocorticoid action. We analyzed physiological and biochemical parameters, adipose tissue histology, insulin sensitivity and lipid metabolism in wild type and MIF-/- C57Bl/6J mice consuming 20% fructose solution for 9 weeks. Glucocorticoid prereceptor metabolism and glucocorticoid receptor (GR) protein level were examined in VAT, together with the expression of glucocorticoid-target genes involved in lipid metabolism. The expression of adipogenic and lipogenic transcriptional regulators peroxisome proliferator activated receptor gamma (PPARG) and sterol regulatory element-binding protein 1c (SREBP1c) was also assessed. Results showed disturbed insulin sensitivity in all MIF-/- mice, regardless of the diet. Mice on fructose diet had increased energy intake, but increased visceral adiposity and enlarged adipocytes were observed only in fructose-fed MIF-/- mice. Increased VAT corticosterone level and 11 beta-hydroxysteroid dehydrogenase type 1, hexose-6-phosphate dehydrogenase and GR protein levels were observed in the same animals, together with induced expression of examined lipogenic genes and accumulation of PPARG and SREBP1c. In conclusion, the results showed that dietary fructose was associated with increased visceral adiposity through activation of GR-regulated lipogenic genes, but only in the absence of MIF, which set the state of hyperinsulinemia and insulin resistance.
T2  - Journal of Endocrinology
T1  - Mif deficiency promotes adiposity in fructose-fed mice.
IS  - 2
VL  - 240
DO  - 10.1530/JOE-18-0333
SP  - 133
EP  - 145
ER  - 

@article{
author = "Gligorovska, Ljupka and Bursać, Biljana and Kovačević, Sanja and Veličković, Nataša and Matić, Gordana and Đorđević, Ana",
year = "2019",
abstract = "The macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine involved in inflammation, regulation of energy metabolism and glucocorticoid action. Chronic low-grade inflammation may be caused by fructose intake, contributing to visceral adipose tissue (VAT) dysfunction. Since MIF is a known antagonist of glucocorticoid signaling, and deregulated glucocorticoid signaling can contribute to lipid metabolism disturbances, we hypothesized that altered MIF signaling might underlie fructose-induced adiposity through glucocorticoid action. We analyzed physiological and biochemical parameters, adipose tissue histology, insulin sensitivity and lipid metabolism in wild type and MIF-/- C57Bl/6J mice consuming 20% fructose solution for 9 weeks. Glucocorticoid prereceptor metabolism and glucocorticoid receptor (GR) protein level were examined in VAT, together with the expression of glucocorticoid-target genes involved in lipid metabolism. The expression of adipogenic and lipogenic transcriptional regulators peroxisome proliferator activated receptor gamma (PPARG) and sterol regulatory element-binding protein 1c (SREBP1c) was also assessed. Results showed disturbed insulin sensitivity in all MIF-/- mice, regardless of the diet. Mice on fructose diet had increased energy intake, but increased visceral adiposity and enlarged adipocytes were observed only in fructose-fed MIF-/- mice. Increased VAT corticosterone level and 11 beta-hydroxysteroid dehydrogenase type 1, hexose-6-phosphate dehydrogenase and GR protein levels were observed in the same animals, together with induced expression of examined lipogenic genes and accumulation of PPARG and SREBP1c. In conclusion, the results showed that dietary fructose was associated with increased visceral adiposity through activation of GR-regulated lipogenic genes, but only in the absence of MIF, which set the state of hyperinsulinemia and insulin resistance.",
journal = "Journal of Endocrinology",
title = "Mif deficiency promotes adiposity in fructose-fed mice.",
number = "2",
volume = "240",
doi = "10.1530/JOE-18-0333",
pages = "133-145"
}

Gligorovska, L., Bursać, B., Kovačević, S., Veličković, N., Matić, G.,& Đorđević, A.. (2019). Mif deficiency promotes adiposity in fructose-fed mice.. in Journal of Endocrinology, 240(2), 133-145.
https://doi.org/10.1530/JOE-18-0333

Gligorovska L, Bursać B, Kovačević S, Veličković N, Matić G, Đorđević A. Mif deficiency promotes adiposity in fructose-fed mice.. in Journal of Endocrinology. 2019;240(2):133-145.
doi:10.1530/JOE-18-0333 .

Gligorovska, Ljupka, Bursać, Biljana, Kovačević, Sanja, Veličković, Nataša, Matić, Gordana, Đorđević, Ana, "Mif deficiency promotes adiposity in fructose-fed mice." in Journal of Endocrinology, 240, no. 2 (2019):133-145,
https://doi.org/10.1530/JOE-18-0333 . .

TY  - CONF
AU  - Veličković, Nataša
AU  - Teofilović, Ana
AU  - Đorđević, Ana
AU  - Vojnović-Milutinović, Danijela
AU  - Bursać, Biljana
AU  - Brkljačić, Jelena
AU  - Elaković, Ivana
AU  - Kovačević, Sanja
AU  - Gligorovska, Ljupka
AU  - Radovanović, Marina
AU  - Preitner, Frederic
AU  - Tappy, Luc
AU  - Matić, Gordana
PY  - 2018
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5253
AB  - The aim: High fructose diet and chronic stress were both
linked with metabolic disturbances. Thus, we analyzed
their separate and combined effects on metabolic ho-
meostasis, with particular focus on hepatic lipogenesis
and gluconeogenesis.
Methods: Male Wistar rats were subjected to 9-week
20% fructose diet and/or 4-week chronic unpredict-
able stress. The following morphological and bio-
chemical parameters of lipid and glucose metabolism
were measured: body and liver mass, energy intake,
blood glucose and plasma insulin levels, free fatty ac-
ids (FFA), lactate, triglycerides (TG) and VLDL-TG, as
well as hepatic VLDL production rate, total hepatic TG
and palmitate and stearate percentage shares. Fur-
thermore, the expression of transcriptional regulators
and enzymes of hepatic de novo lipogenesis (DNL), li-
poprotein export and gluconeogenesis were analyzed.
Results: Although energy intake was increased after
fructose diet, body and liver mass remained unaltered.
Plasma TG were elevated in both fructose-fed groups,
whereas FFA were increased in the non-stressed fruc-
tose-fed group. Parameters of hepatic TG and VLDL
production and export were unaffected, except for the
hepatic palmitate production which was increased after
combined treatment. The increments of fractional DNL
and palmitate production accompanied the upregu-
lation of lipogenic enzymes, fatty acid sythase and
acetyl-CoA carboxylase, which was, interestingly, not
preceeded by the increase of their transcriptional reg-
ulators. In both fructose-fed groups blood glucose level
was increased, although hepatic gluconeogenesis
was unaffected.
Conclusion: Combined stress/fructose treatment is
more aggravating than separate treatments, since it
leads to an increase in hepatic de novo lipogenesis
and total hepatic TG palmitate, without concomitant
changes in VLDL production and export.
PB  - Belgrade: Institute for Biological Research "Siniša Stanković"– National Institute of Republic of Serbia, University of Belgrade
C3  - Program & Book of Abstracts: IUBMB Advanced School Nutrition, Metabolism and Aging; 2018 Oct 15-19; Petnica, Serbia.
T1  - De novo lipogenesis and gluconeogenesis in the liver of male fructose-fed rats exposed to chronic stress
SP  - 18
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5253
ER  - 

@conference{
author = "Veličković, Nataša and Teofilović, Ana and Đorđević, Ana and Vojnović-Milutinović, Danijela and Bursać, Biljana and Brkljačić, Jelena and Elaković, Ivana and Kovačević, Sanja and Gligorovska, Ljupka and Radovanović, Marina and Preitner, Frederic and Tappy, Luc and Matić, Gordana",
year = "2018",
abstract = "The aim: High fructose diet and chronic stress were both
linked with metabolic disturbances. Thus, we analyzed
their separate and combined effects on metabolic ho-
meostasis, with particular focus on hepatic lipogenesis
and gluconeogenesis.
Methods: Male Wistar rats were subjected to 9-week
20% fructose diet and/or 4-week chronic unpredict-
able stress. The following morphological and bio-
chemical parameters of lipid and glucose metabolism
were measured: body and liver mass, energy intake,
blood glucose and plasma insulin levels, free fatty ac-
ids (FFA), lactate, triglycerides (TG) and VLDL-TG, as
well as hepatic VLDL production rate, total hepatic TG
and palmitate and stearate percentage shares. Fur-
thermore, the expression of transcriptional regulators
and enzymes of hepatic de novo lipogenesis (DNL), li-
poprotein export and gluconeogenesis were analyzed.
Results: Although energy intake was increased after
fructose diet, body and liver mass remained unaltered.
Plasma TG were elevated in both fructose-fed groups,
whereas FFA were increased in the non-stressed fruc-
tose-fed group. Parameters of hepatic TG and VLDL
production and export were unaffected, except for the
hepatic palmitate production which was increased after
combined treatment. The increments of fractional DNL
and palmitate production accompanied the upregu-
lation of lipogenic enzymes, fatty acid sythase and
acetyl-CoA carboxylase, which was, interestingly, not
preceeded by the increase of their transcriptional reg-
ulators. In both fructose-fed groups blood glucose level
was increased, although hepatic gluconeogenesis
was unaffected.
Conclusion: Combined stress/fructose treatment is
more aggravating than separate treatments, since it
leads to an increase in hepatic de novo lipogenesis
and total hepatic TG palmitate, without concomitant
changes in VLDL production and export.",
publisher = "Belgrade: Institute for Biological Research "Siniša Stanković"– National Institute of Republic of Serbia, University of Belgrade",
journal = "Program & Book of Abstracts: IUBMB Advanced School Nutrition, Metabolism and Aging; 2018 Oct 15-19; Petnica, Serbia.",
title = "De novo lipogenesis and gluconeogenesis in the liver of male fructose-fed rats exposed to chronic stress",
pages = "18",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5253"
}

Veličković, N., Teofilović, A., Đorđević, A., Vojnović-Milutinović, D., Bursać, B., Brkljačić, J., Elaković, I., Kovačević, S., Gligorovska, L., Radovanović, M., Preitner, F., Tappy, L.,& Matić, G.. (2018). De novo lipogenesis and gluconeogenesis in the liver of male fructose-fed rats exposed to chronic stress. in Program & Book of Abstracts: IUBMB Advanced School Nutrition, Metabolism and Aging; 2018 Oct 15-19; Petnica, Serbia.
Belgrade: Institute for Biological Research "Siniša Stanković"– National Institute of Republic of Serbia, University of Belgrade., 18.
https://hdl.handle.net/21.15107/rcub_ibiss_5253

Veličković N, Teofilović A, Đorđević A, Vojnović-Milutinović D, Bursać B, Brkljačić J, Elaković I, Kovačević S, Gligorovska L, Radovanović M, Preitner F, Tappy L, Matić G. De novo lipogenesis and gluconeogenesis in the liver of male fructose-fed rats exposed to chronic stress. in Program & Book of Abstracts: IUBMB Advanced School Nutrition, Metabolism and Aging; 2018 Oct 15-19; Petnica, Serbia.. 2018;:18.
https://hdl.handle.net/21.15107/rcub_ibiss_5253 .

Veličković, Nataša, Teofilović, Ana, Đorđević, Ana, Vojnović-Milutinović, Danijela, Bursać, Biljana, Brkljačić, Jelena, Elaković, Ivana, Kovačević, Sanja, Gligorovska, Ljupka, Radovanović, Marina, Preitner, Frederic, Tappy, Luc, Matić, Gordana, "De novo lipogenesis and gluconeogenesis in the liver of male fructose-fed rats exposed to chronic stress" in Program & Book of Abstracts: IUBMB Advanced School Nutrition, Metabolism and Aging; 2018 Oct 15-19; Petnica, Serbia. (2018):18,
https://hdl.handle.net/21.15107/rcub_ibiss_5253 .

TY  - JOUR
AU  - Bursać, Biljana
AU  - Đorđević, Ana
AU  - Veličković, Nataša
AU  - Vojnović-Milutinović, Danijela
AU  - Petrović, Snježana
AU  - Teofilović, Ana
AU  - Gligorovska, Ljupka
AU  - Preitner, Frederic
AU  - Tappy, Luc
AU  - Matić, Gordana
PY  - 2018
UR  - https://www.sciencedirect.com/science/article/pii/S0303720718301345?via%3Dihub
UR  - http://www.ncbi.nlm.nih.gov/pubmed/29729371
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3060
AB  - Both fructose overconsumption and increased glucocorticoids secondary to chronic stress may contribute to overall dyslipidemia. In this study we specifically assessed the effects and interactions of dietary fructose and chronic stress on lipid metabolism in the visceral adipose tissue (VAT) of male Wistar rats. We analyzed the effects of 9-week 20% high fructose diet and 4-week chronic unpredictable stress, separately and in combination, on VAT histology, glucocorticoid prereceptor metabolism, glucocorticoid receptor subcellular redistribution and expression of major metabolic genes. Blood triglycerides and fatty acid composition were also measured to assess hepatic Δ9 desaturase activity. The results showed that fructose diet increased blood triglycerides and Δ9 desaturase activity. On the other hand, stress led to corticosterone elevation, glucocorticoid receptor activation and decrease in adipocyte size, while phosphoenolpyruvate carboxykinase, adipose tissue triglyceride lipase, FAT/CD36 and sterol regulatory element binding protein-1c (SREBP-1c) were increased, pointing to VAT lipolysis and glyceroneogenesis. The combination of stress and fructose diet was associated with marked stimulation of fatty acid synthase and acetyl-CoA carboxylase mRNA level and with increased 11β-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase protein levels, suggesting a coordinated increase in hexose monophosphate shunt and de novo lipogenesis. It however did not influence the level of peroxisome proliferator-activated receptor-gamma, SREBP-1c and carbohydrate responsive element-binding protein. In conclusion, our results showed that only combination of dietary fructose and stress increase glucocorticoid prereceptor metabolism and stimulates lipogenic enzyme expression suggesting that interaction between stress and fructose may be instrumental in promoting VAT expansion and dysfunction.
T2  - Molecular and Cellular Endocrinology
T1  - Involvement of glucocorticoid prereceptor metabolism and signaling in rat visceral adipose tissue lipid metabolism after chronic stress combined with high-fructose diet.
DO  - 10.1016/j.mce.2018.04.015
ER  - 

@article{
author = "Bursać, Biljana and Đorđević, Ana and Veličković, Nataša and Vojnović-Milutinović, Danijela and Petrović, Snježana and Teofilović, Ana and Gligorovska, Ljupka and Preitner, Frederic and Tappy, Luc and Matić, Gordana",
year = "2018",
abstract = "Both fructose overconsumption and increased glucocorticoids secondary to chronic stress may contribute to overall dyslipidemia. In this study we specifically assessed the effects and interactions of dietary fructose and chronic stress on lipid metabolism in the visceral adipose tissue (VAT) of male Wistar rats. We analyzed the effects of 9-week 20% high fructose diet and 4-week chronic unpredictable stress, separately and in combination, on VAT histology, glucocorticoid prereceptor metabolism, glucocorticoid receptor subcellular redistribution and expression of major metabolic genes. Blood triglycerides and fatty acid composition were also measured to assess hepatic Δ9 desaturase activity. The results showed that fructose diet increased blood triglycerides and Δ9 desaturase activity. On the other hand, stress led to corticosterone elevation, glucocorticoid receptor activation and decrease in adipocyte size, while phosphoenolpyruvate carboxykinase, adipose tissue triglyceride lipase, FAT/CD36 and sterol regulatory element binding protein-1c (SREBP-1c) were increased, pointing to VAT lipolysis and glyceroneogenesis. The combination of stress and fructose diet was associated with marked stimulation of fatty acid synthase and acetyl-CoA carboxylase mRNA level and with increased 11β-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase protein levels, suggesting a coordinated increase in hexose monophosphate shunt and de novo lipogenesis. It however did not influence the level of peroxisome proliferator-activated receptor-gamma, SREBP-1c and carbohydrate responsive element-binding protein. In conclusion, our results showed that only combination of dietary fructose and stress increase glucocorticoid prereceptor metabolism and stimulates lipogenic enzyme expression suggesting that interaction between stress and fructose may be instrumental in promoting VAT expansion and dysfunction.",
journal = "Molecular and Cellular Endocrinology",
title = "Involvement of glucocorticoid prereceptor metabolism and signaling in rat visceral adipose tissue lipid metabolism after chronic stress combined with high-fructose diet.",
doi = "10.1016/j.mce.2018.04.015"
}

Bursać, B., Đorđević, A., Veličković, N., Vojnović-Milutinović, D., Petrović, S., Teofilović, A., Gligorovska, L., Preitner, F., Tappy, L.,& Matić, G.. (2018). Involvement of glucocorticoid prereceptor metabolism and signaling in rat visceral adipose tissue lipid metabolism after chronic stress combined with high-fructose diet.. in Molecular and Cellular Endocrinology.
https://doi.org/10.1016/j.mce.2018.04.015

Bursać B, Đorđević A, Veličković N, Vojnović-Milutinović D, Petrović S, Teofilović A, Gligorovska L, Preitner F, Tappy L, Matić G. Involvement of glucocorticoid prereceptor metabolism and signaling in rat visceral adipose tissue lipid metabolism after chronic stress combined with high-fructose diet.. in Molecular and Cellular Endocrinology. 2018;.
doi:10.1016/j.mce.2018.04.015 .

Bursać, Biljana, Đorđević, Ana, Veličković, Nataša, Vojnović-Milutinović, Danijela, Petrović, Snježana, Teofilović, Ana, Gligorovska, Ljupka, Preitner, Frederic, Tappy, Luc, Matić, Gordana, "Involvement of glucocorticoid prereceptor metabolism and signaling in rat visceral adipose tissue lipid metabolism after chronic stress combined with high-fructose diet." in Molecular and Cellular Endocrinology (2018),
https://doi.org/10.1016/j.mce.2018.04.015 . .

TY  - JOUR
AU  - Vojnović Milutinović, Danijela
AU  - Radovanović, Marina
AU  - Veličković, Nataša
AU  - Đorđević, Ana
AU  - Bursać, Biljana
AU  - Brkljačić, Jelena
AU  - Teofilović, Ana
AU  - Božić Antić, Ivana
AU  - Bjekić-Macut, Jelica
AU  - Shirif Zidane, Abdulbaset
AU  - Matić, Gordana
AU  - Macut, Đuro
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6331
AB  - Polycystic ovary syndrome is a heterogeneous endocrine and metabolic disorder associated with abdominal obesity, dyslipidemia and insulin resistance. Since abdominal obesity is characterized by low-grade inflammation, the aim of the study was to investigate whether visceral adipose tissue inflammation linked to abdominal obesity and dyslipidemia could lead to impaired insulin sensitivity in the animal model of polycystic ovary syndrome. 
Female Wistar rats were treated with nonaromatizable 5α dihydrotestosterone pellets in order to induce reproductive and metabolic characteristics of polycystic ovary syndrome. Glucose, triglycerides, non-esterified fatty acids and insulin were determined in blood plasma. Visceral adipose tissue inflammation was evaluated by the nuclear factor kappa B intracellular distribution, macrophage migration inhibitory factor protein level, as well as TNFα, IL6 and IL1β mRNA levels. Insulin sensitivity was assessed by intraperitoneal glucose tolerance test and homeostasis model assessment index, and through analysis of insulin signaling pathway in the visceral adipose tissue.
Dihydrotestosterone treatment led to increased body weight, abdominal obesity and elevated triglycerides and non-esterified fatty acids, which were accompanied by the activation of nuclear factor kappa B and increase in macrophage migration inhibitory factor, IL6 and IL1β levels in the visceral adipose tissue. In parallel, insulin sensitivity was affected in 5α dihydrotestosterone-treated animals only at the systemic, and not at the level of visceral adipose tissue. 
The results showed that abdominal obesity and dyslipidemia in the animal model of polycystic ovary syndrome were accompanied with low-grade inflammation in the visceral adipose tissue. However, these metabolic disturbances did not result in decreased tissue insulin sensitivity.
PB  - Stuttgart: Georg Thieme Verlag KG
T2  - Experimental and Clinical Endocrinology and Diabetes
T1  - Enhanced inflammation without impairment of insulin signaling in the visceral adipose tissue of 5α- dihydrotestosterone-induced animal model of polycystic ovary syndrome
IS  - 8
VL  - 125
DO  - 10.1055/s-0043-104531
SP  - 522
EP  - 529
ER  - 

@article{
author = "Vojnović Milutinović, Danijela and Radovanović, Marina and Veličković, Nataša and Đorđević, Ana and Bursać, Biljana and Brkljačić, Jelena and Teofilović, Ana and Božić Antić, Ivana and Bjekić-Macut, Jelica and Shirif Zidane, Abdulbaset and Matić, Gordana and Macut, Đuro",
year = "2017",
abstract = "Polycystic ovary syndrome is a heterogeneous endocrine and metabolic disorder associated with abdominal obesity, dyslipidemia and insulin resistance. Since abdominal obesity is characterized by low-grade inflammation, the aim of the study was to investigate whether visceral adipose tissue inflammation linked to abdominal obesity and dyslipidemia could lead to impaired insulin sensitivity in the animal model of polycystic ovary syndrome. 
Female Wistar rats were treated with nonaromatizable 5α dihydrotestosterone pellets in order to induce reproductive and metabolic characteristics of polycystic ovary syndrome. Glucose, triglycerides, non-esterified fatty acids and insulin were determined in blood plasma. Visceral adipose tissue inflammation was evaluated by the nuclear factor kappa B intracellular distribution, macrophage migration inhibitory factor protein level, as well as TNFα, IL6 and IL1β mRNA levels. Insulin sensitivity was assessed by intraperitoneal glucose tolerance test and homeostasis model assessment index, and through analysis of insulin signaling pathway in the visceral adipose tissue.
Dihydrotestosterone treatment led to increased body weight, abdominal obesity and elevated triglycerides and non-esterified fatty acids, which were accompanied by the activation of nuclear factor kappa B and increase in macrophage migration inhibitory factor, IL6 and IL1β levels in the visceral adipose tissue. In parallel, insulin sensitivity was affected in 5α dihydrotestosterone-treated animals only at the systemic, and not at the level of visceral adipose tissue. 
The results showed that abdominal obesity and dyslipidemia in the animal model of polycystic ovary syndrome were accompanied with low-grade inflammation in the visceral adipose tissue. However, these metabolic disturbances did not result in decreased tissue insulin sensitivity.",
publisher = "Stuttgart: Georg Thieme Verlag KG",
journal = "Experimental and Clinical Endocrinology and Diabetes",
title = "Enhanced inflammation without impairment of insulin signaling in the visceral adipose tissue of 5α- dihydrotestosterone-induced animal model of polycystic ovary syndrome",
number = "8",
volume = "125",
doi = "10.1055/s-0043-104531",
pages = "522-529"
}

Vojnović Milutinović, D., Radovanović, M., Veličković, N., Đorđević, A., Bursać, B., Brkljačić, J., Teofilović, A., Božić Antić, I., Bjekić-Macut, J., Shirif Zidane, A., Matić, G.,& Macut, Đ.. (2017). Enhanced inflammation without impairment of insulin signaling in the visceral adipose tissue of 5α- dihydrotestosterone-induced animal model of polycystic ovary syndrome. in Experimental and Clinical Endocrinology and Diabetes
Stuttgart: Georg Thieme Verlag KG., 125(8), 522-529.
https://doi.org/10.1055/s-0043-104531

Vojnović Milutinović D, Radovanović M, Veličković N, Đorđević A, Bursać B, Brkljačić J, Teofilović A, Božić Antić I, Bjekić-Macut J, Shirif Zidane A, Matić G, Macut Đ. Enhanced inflammation without impairment of insulin signaling in the visceral adipose tissue of 5α- dihydrotestosterone-induced animal model of polycystic ovary syndrome. in Experimental and Clinical Endocrinology and Diabetes. 2017;125(8):522-529.
doi:10.1055/s-0043-104531 .

Vojnović Milutinović, Danijela, Radovanović, Marina, Veličković, Nataša, Đorđević, Ana, Bursać, Biljana, Brkljačić, Jelena, Teofilović, Ana, Božić Antić, Ivana, Bjekić-Macut, Jelica, Shirif Zidane, Abdulbaset, Matić, Gordana, Macut, Đuro, "Enhanced inflammation without impairment of insulin signaling in the visceral adipose tissue of 5α- dihydrotestosterone-induced animal model of polycystic ovary syndrome" in Experimental and Clinical Endocrinology and Diabetes, 125, no. 8 (2017):522-529,
https://doi.org/10.1055/s-0043-104531 . .

TY  - CONF
AU  - Gligorovska, Ljupka
AU  - Đorđević, Ana
AU  - Bursać, Biljana
AU  - Teofilović, Ana
AU  - Veličković, Nataša
AU  - Vojnović-Milutinović, Danijela
AU  - Kovačević, Sanja
AU  - Matić, Gordana
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5257
AB  - Introduction: The macrophage migration inhibitory factor (MIF) is a pro-inflammatory
cytokine involved in metabolic inflammation and regulation of glucocorticoid
action. Low-grade inflammation in adipose tissue is associated with obesity and
dyslipidemia and may be caused by fructose-enriched diet. We hypothesized that
the effects of MIF deficiency on lipid metabolism in adipose tissue, after high fructose
consumption, could be mediated by glucocorticoids (GCs) as potent regulators of
energy metabolism.
Methods: We analyzed the effects of 9-week 20% fructose-enriched diet on energy
intake, body mass, intra-abdominal adipose tissue mass and histology in MIF wild
type (WT) and MIF deficient (MIF−/−) C57Bl/6J mice. Expression of key transcriptional
regulators involved in adipogenesis and lipogenesis, peroxisome-proliferator-
activated receptor γ (PPARγ) and sterol regulatory element-binding protein-1
(SREBP-1), was also assessed. Glucocorticoid signaling was characterized by
prereceptor metabolism, glucocorticoid receptor (GR) protein level and
phosphorylation, and expression of GC-target genes involved in lipogenesis.
Results: Both WT and MIF−/− mice on fructose diet had increased energy intake, but
the elevation of adipose tissue mass and enlargement of adipocytes were observed
only in fructose-fed MIF−/− mice. Elevated GR protein level and its activating Ser220
phosphorylation, enhanced glucocorticoid prereceptor metabolism, an increase in
PPARγ and SREBP-1 levels and induced expression of all examined lipogenic genes
were also observed in MIF−/− mice on fructose diet.
Conclusion: The results show that only under fructose caloric overload MIF deficiency
results in lipogenesis and adipocyte hyperthrophy and that this effect might be
mediated by enhanced glucocorticoid signalling in intra-abdominal adipose tissue
PB  - Belgrade: University of Belgrade, Faculty of Biology
C3  - Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
T1  - Glucocorticoid-mediated effects of MIF deficiency and fructose-enriched diet on lipid metabolism in the mouse intra-abdominal adipose tissue
SP  - 38
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5257
ER  - 

@conference{
author = "Gligorovska, Ljupka and Đorđević, Ana and Bursać, Biljana and Teofilović, Ana and Veličković, Nataša and Vojnović-Milutinović, Danijela and Kovačević, Sanja and Matić, Gordana",
year = "2017",
abstract = "Introduction: The macrophage migration inhibitory factor (MIF) is a pro-inflammatory
cytokine involved in metabolic inflammation and regulation of glucocorticoid
action. Low-grade inflammation in adipose tissue is associated with obesity and
dyslipidemia and may be caused by fructose-enriched diet. We hypothesized that
the effects of MIF deficiency on lipid metabolism in adipose tissue, after high fructose
consumption, could be mediated by glucocorticoids (GCs) as potent regulators of
energy metabolism.
Methods: We analyzed the effects of 9-week 20% fructose-enriched diet on energy
intake, body mass, intra-abdominal adipose tissue mass and histology in MIF wild
type (WT) and MIF deficient (MIF−/−) C57Bl/6J mice. Expression of key transcriptional
regulators involved in adipogenesis and lipogenesis, peroxisome-proliferator-
activated receptor γ (PPARγ) and sterol regulatory element-binding protein-1
(SREBP-1), was also assessed. Glucocorticoid signaling was characterized by
prereceptor metabolism, glucocorticoid receptor (GR) protein level and
phosphorylation, and expression of GC-target genes involved in lipogenesis.
Results: Both WT and MIF−/− mice on fructose diet had increased energy intake, but
the elevation of adipose tissue mass and enlargement of adipocytes were observed
only in fructose-fed MIF−/− mice. Elevated GR protein level and its activating Ser220
phosphorylation, enhanced glucocorticoid prereceptor metabolism, an increase in
PPARγ and SREBP-1 levels and induced expression of all examined lipogenic genes
were also observed in MIF−/− mice on fructose diet.
Conclusion: The results show that only under fructose caloric overload MIF deficiency
results in lipogenesis and adipocyte hyperthrophy and that this effect might be
mediated by enhanced glucocorticoid signalling in intra-abdominal adipose tissue",
publisher = "Belgrade: University of Belgrade, Faculty of Biology",
journal = "Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.",
title = "Glucocorticoid-mediated effects of MIF deficiency and fructose-enriched diet on lipid metabolism in the mouse intra-abdominal adipose tissue",
pages = "38",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5257"
}

Gligorovska, L., Đorđević, A., Bursać, B., Teofilović, A., Veličković, N., Vojnović-Milutinović, D., Kovačević, S.,& Matić, G.. (2017). Glucocorticoid-mediated effects of MIF deficiency and fructose-enriched diet on lipid metabolism in the mouse intra-abdominal adipose tissue. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
Belgrade: University of Belgrade, Faculty of Biology., 38.
https://hdl.handle.net/21.15107/rcub_ibiss_5257

Gligorovska L, Đorđević A, Bursać B, Teofilović A, Veličković N, Vojnović-Milutinović D, Kovačević S, Matić G. Glucocorticoid-mediated effects of MIF deficiency and fructose-enriched diet on lipid metabolism in the mouse intra-abdominal adipose tissue. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.. 2017;:38.
https://hdl.handle.net/21.15107/rcub_ibiss_5257 .

Gligorovska, Ljupka, Đorđević, Ana, Bursać, Biljana, Teofilović, Ana, Veličković, Nataša, Vojnović-Milutinović, Danijela, Kovačević, Sanja, Matić, Gordana, "Glucocorticoid-mediated effects of MIF deficiency and fructose-enriched diet on lipid metabolism in the mouse intra-abdominal adipose tissue" in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia. (2017):38,
https://hdl.handle.net/21.15107/rcub_ibiss_5257 .

TY  - CONF
AU  - Gligorovska, Ljupka
AU  - Đorđević, Ana
AU  - Bursać, Biljana
AU  - Veličković, Nataša
AU  - Ignjatović, Đurđica
AU  - Tomić, Mirko
AU  - Matić, Gordana
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5443
AB  - Introduction: The macrophage migration inhibitory factor (MIF) is involved in the regulation of glucose metabolism in the hippocampus, while fructose overconsumption has been associated with changes in hippocampal insulin sensitivity and synaptic plasticity, resulting in disturbances in learning and memory. Therefore, we hypothesized that MIF defficiency in combination with fructose diet (FD) may affect insulin sensitivity and hippocampal synaptic plasticity, thus leading to behavioral changes.
Methods: The effects of 9-week 20% FD on energy intake and insulin sensitivity in wild type (WT) and MIF deficient (MIF−/−) C57Bl/6J male mice were analyzed. Inhibitory Ser307 phosphorylation of insulin receptor substrate 1 (IRS-1) was used as hallmark of hippocampal insulin resistance. Novel object recognition test (NOR) was used to assess exploratory behavior. Synaptic plasticity was estimated by polysialylated-neural cell adhesion molecule (PSA-NCAM) protein level.
Results: WT and MIF−/− mice on fructose diet had increased energy intake, while systemic insulin sensitivity was disturbed in all MIF−/− mice. Hippocampal pIRS-1 Ser307 was elevated in all animals compared to WT on standard diet (SD). MIF−/− animals on SD showed impaired recognition memory in NOR. Finally, although PSA-NCAM was decreased in WT animals on FD and MIF−/− on SD, its level in fructose-fed MIF−/− mice was the same as in the WT on SD.
Conclusion: These preliminary results show that both MIF defficiency and fructose caloric overload are implicated in impairment of systemic and hippocampal insulin sensitivity. However, behavioral changes observed in MIF−/− mice were normalized after fructose feeding, which coincided with the changes in synaptosomal PSA-NCAM protein level.
PB  - Belgrade: Serbian Neuroscience Society
C3  - Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia
T1  - Effects of macrophage migration inhibitory factor deficiency and fructose-enriched diet on systemic and hippocampal insulin sesitivity, behavior and hippocampal plasticity in male mice
SP  - 97
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5443
ER  - 

@conference{
author = "Gligorovska, Ljupka and Đorđević, Ana and Bursać, Biljana and Veličković, Nataša and Ignjatović, Đurđica and Tomić, Mirko and Matić, Gordana",
year = "2017",
abstract = "Introduction: The macrophage migration inhibitory factor (MIF) is involved in the regulation of glucose metabolism in the hippocampus, while fructose overconsumption has been associated with changes in hippocampal insulin sensitivity and synaptic plasticity, resulting in disturbances in learning and memory. Therefore, we hypothesized that MIF defficiency in combination with fructose diet (FD) may affect insulin sensitivity and hippocampal synaptic plasticity, thus leading to behavioral changes.
Methods: The effects of 9-week 20% FD on energy intake and insulin sensitivity in wild type (WT) and MIF deficient (MIF−/−) C57Bl/6J male mice were analyzed. Inhibitory Ser307 phosphorylation of insulin receptor substrate 1 (IRS-1) was used as hallmark of hippocampal insulin resistance. Novel object recognition test (NOR) was used to assess exploratory behavior. Synaptic plasticity was estimated by polysialylated-neural cell adhesion molecule (PSA-NCAM) protein level.
Results: WT and MIF−/− mice on fructose diet had increased energy intake, while systemic insulin sensitivity was disturbed in all MIF−/− mice. Hippocampal pIRS-1 Ser307 was elevated in all animals compared to WT on standard diet (SD). MIF−/− animals on SD showed impaired recognition memory in NOR. Finally, although PSA-NCAM was decreased in WT animals on FD and MIF−/− on SD, its level in fructose-fed MIF−/− mice was the same as in the WT on SD.
Conclusion: These preliminary results show that both MIF defficiency and fructose caloric overload are implicated in impairment of systemic and hippocampal insulin sensitivity. However, behavioral changes observed in MIF−/− mice were normalized after fructose feeding, which coincided with the changes in synaptosomal PSA-NCAM protein level.",
publisher = "Belgrade: Serbian Neuroscience Society",
journal = "Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia",
title = "Effects of macrophage migration inhibitory factor deficiency and fructose-enriched diet on systemic and hippocampal insulin sesitivity, behavior and hippocampal plasticity in male mice",
pages = "97",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5443"
}

Gligorovska, L., Đorđević, A., Bursać, B., Veličković, N., Ignjatović, Đ., Tomić, M.,& Matić, G.. (2017). Effects of macrophage migration inhibitory factor deficiency and fructose-enriched diet on systemic and hippocampal insulin sesitivity, behavior and hippocampal plasticity in male mice. in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia
Belgrade: Serbian Neuroscience Society., 97.
https://hdl.handle.net/21.15107/rcub_ibiss_5443

Gligorovska L, Đorđević A, Bursać B, Veličković N, Ignjatović Đ, Tomić M, Matić G. Effects of macrophage migration inhibitory factor deficiency and fructose-enriched diet on systemic and hippocampal insulin sesitivity, behavior and hippocampal plasticity in male mice. in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia. 2017;:97.
https://hdl.handle.net/21.15107/rcub_ibiss_5443 .

Gligorovska, Ljupka, Đorđević, Ana, Bursać, Biljana, Veličković, Nataša, Ignjatović, Đurđica, Tomić, Mirko, Matić, Gordana, "Effects of macrophage migration inhibitory factor deficiency and fructose-enriched diet on systemic and hippocampal insulin sesitivity, behavior and hippocampal plasticity in male mice" in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia (2017):97,
https://hdl.handle.net/21.15107/rcub_ibiss_5443 .

TY  - JOUR
AU  - Bundalo, Maja
AU  - Đorđević, Ana
AU  - Bursać, Biljana
AU  - Živković, Maja
AU  - Korićanac, Goran
AU  - Stanković, Aleksandra
PY  - 2017
UR  - http://www.nrcresearchpress.com/doi/10.1139/apnm-2016-0725
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2936
AB  - The adipose tissue renin–angiotensin system (RAS) is proposed to be a pathophysiological link between adipose tissue dysregulation and metabolic disorders induced by a fructose-rich diet (FRD). RAS can act intracellularly. We hypothesized that adipocyte nuclear membranes possess angiotensin receptor types 1 and 2 (AT1R and AT2R), which couple to nuclear signaling pathways and regulate oxidative gene expression under FRD conditions. We analyzed the effect of consumption of 10% fructose solution for 9 weeks on biochemical parameters, adipocyte morphology, and expression of AT1R, AT2R, AT1R-associated protein (ATRAP), NADPH oxidase 4 (NOX4), matrix metalloproteinase-9 (MMP-9), and manganese superoxide dismutase (MnSOD) in adipose tissue of Wistar rats. We detected AT1R and AT2R in the nuclear fraction. FRD reduced the level of angiotensin receptors in the nucleus, while increased AT1R and decreased AT2R levels were observed in the plasma membrane. FRD increased the ATRAP mRNA level and decreased MnSOD mRNA and protein levels. No significant differences were observed for MMP-9 and NOX4 mRNA levels. These findings coincided with hyperleptinemia, elevated blood pressure and triglycerides, and unchanged visceral adipose tissue mass and morphology in FRD rats. Besides providing evidence for nuclear localization of angiotensin receptors in visceral adipose tissue, this study demonstrates the different effects of FRD on AT1R expression in different cellular compartments. Elevated blood pressure and decreased antioxidant capacity in visceral fat of fructose-fed rats were accompanied by an increased AT1R level in the plasma membrane, while upregulation of ATRAP and a decrease of nuclear membrane AT1R suggest an increased capacity for attenuation of excessive AT1R signaling and visceral adiposity.
T2  - Applied Physiology, Nutrition, and Metabolism
T2  - Applied Physiology, Nutrition, and Metabolism
T1  - Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue
IS  - 12
VL  - 42
DO  - 10.1139/apnm-2016-0725
SP  - 1254
EP  - 1263
ER  - 

@article{
author = "Bundalo, Maja and Đorđević, Ana and Bursać, Biljana and Živković, Maja and Korićanac, Goran and Stanković, Aleksandra",
year = "2017",
abstract = "The adipose tissue renin–angiotensin system (RAS) is proposed to be a pathophysiological link between adipose tissue dysregulation and metabolic disorders induced by a fructose-rich diet (FRD). RAS can act intracellularly. We hypothesized that adipocyte nuclear membranes possess angiotensin receptor types 1 and 2 (AT1R and AT2R), which couple to nuclear signaling pathways and regulate oxidative gene expression under FRD conditions. We analyzed the effect of consumption of 10% fructose solution for 9 weeks on biochemical parameters, adipocyte morphology, and expression of AT1R, AT2R, AT1R-associated protein (ATRAP), NADPH oxidase 4 (NOX4), matrix metalloproteinase-9 (MMP-9), and manganese superoxide dismutase (MnSOD) in adipose tissue of Wistar rats. We detected AT1R and AT2R in the nuclear fraction. FRD reduced the level of angiotensin receptors in the nucleus, while increased AT1R and decreased AT2R levels were observed in the plasma membrane. FRD increased the ATRAP mRNA level and decreased MnSOD mRNA and protein levels. No significant differences were observed for MMP-9 and NOX4 mRNA levels. These findings coincided with hyperleptinemia, elevated blood pressure and triglycerides, and unchanged visceral adipose tissue mass and morphology in FRD rats. Besides providing evidence for nuclear localization of angiotensin receptors in visceral adipose tissue, this study demonstrates the different effects of FRD on AT1R expression in different cellular compartments. Elevated blood pressure and decreased antioxidant capacity in visceral fat of fructose-fed rats were accompanied by an increased AT1R level in the plasma membrane, while upregulation of ATRAP and a decrease of nuclear membrane AT1R suggest an increased capacity for attenuation of excessive AT1R signaling and visceral adiposity.",
journal = "Applied Physiology, Nutrition, and Metabolism, Applied Physiology, Nutrition, and Metabolism",
title = "Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue",
number = "12",
volume = "42",
doi = "10.1139/apnm-2016-0725",
pages = "1254-1263"
}

Bundalo, M., Đorđević, A., Bursać, B., Živković, M., Korićanac, G.,& Stanković, A.. (2017). Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue. in Applied Physiology, Nutrition, and Metabolism, 42(12), 1254-1263.
https://doi.org/10.1139/apnm-2016-0725

Bundalo M, Đorđević A, Bursać B, Živković M, Korićanac G, Stanković A. Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue. in Applied Physiology, Nutrition, and Metabolism. 2017;42(12):1254-1263.
doi:10.1139/apnm-2016-0725 .

Bundalo, Maja, Đorđević, Ana, Bursać, Biljana, Živković, Maja, Korićanac, Goran, Stanković, Aleksandra, "Fructose-rich diet differently affects angiotensin II receptor content in the nucleus and a plasma membrane fraction of visceral adipose tissue" in Applied Physiology, Nutrition, and Metabolism, 42, no. 12 (2017):1254-1263,
https://doi.org/10.1139/apnm-2016-0725 . .