TY  - JOUR
AU  - Paunović, Marija
AU  - Milošević, Maja
AU  - Mitrović-Ajtić, Olivera
AU  - Veličković, Nataša
AU  - Mićić, Bojana
AU  - Nedić, Olgica
AU  - Todorović, Vanja
AU  - Vučić, Vesna
AU  - Petrović, Snježana
PY  - 2024
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6684
AB  - Diets high in fat and sugar lead to metabolic syndrome (MetS) and related chronic diseases. We
investigated the effects of commercially available, cold-pressed polyphenol-rich black currant
(BC) and cornelian cherry (CC) juices on the prevention of MetS in Wistar rats induced by a 10-
weeks high-fat high-fructose (HFF) diet. Juice consumption, either BC or CC, with a HFF diet
resulted in lower serum triglycerides compared to only the HFF consumption. Both juices also
mitigated the effects of HFF on the liver, pancreas, and adipose tissue, by preserving liver and
pancreas histomorphology and reducing visceral fat and adipocyte size. Furthermore, supple-
mentation with both juices reduced glucagon and up-regulated insulin expression in the pancreas
of the rats on the HFF diet, whereas the BC also showed improved glucose regulation. BC juice
also reduced the expression of IL-6 and hepatic inflammation compared to the group only on HFF
diet. Both juices, especially BC, could be a convenient solution for the prevention of MetS in
humans.
PB  - Elsevier Ltd.
T2  - Heliyon
T1  - Polyphenol-rich black currant and cornelian cherry juices ameliorate metabolic syndrome induced by a high-fat high-fructose diet in Wistar rats
IS  - 7
VL  - 10
DO  - 10.1016/j.heliyon.2024.e27709
SP  - e27709
ER  - 

@article{
author = "Paunović, Marija and Milošević, Maja and Mitrović-Ajtić, Olivera and Veličković, Nataša and Mićić, Bojana and Nedić, Olgica and Todorović, Vanja and Vučić, Vesna and Petrović, Snježana",
year = "2024",
abstract = "Diets high in fat and sugar lead to metabolic syndrome (MetS) and related chronic diseases. We
investigated the effects of commercially available, cold-pressed polyphenol-rich black currant
(BC) and cornelian cherry (CC) juices on the prevention of MetS in Wistar rats induced by a 10-
weeks high-fat high-fructose (HFF) diet. Juice consumption, either BC or CC, with a HFF diet
resulted in lower serum triglycerides compared to only the HFF consumption. Both juices also
mitigated the effects of HFF on the liver, pancreas, and adipose tissue, by preserving liver and
pancreas histomorphology and reducing visceral fat and adipocyte size. Furthermore, supple-
mentation with both juices reduced glucagon and up-regulated insulin expression in the pancreas
of the rats on the HFF diet, whereas the BC also showed improved glucose regulation. BC juice
also reduced the expression of IL-6 and hepatic inflammation compared to the group only on HFF
diet. Both juices, especially BC, could be a convenient solution for the prevention of MetS in
humans.",
publisher = "Elsevier Ltd.",
journal = "Heliyon",
title = "Polyphenol-rich black currant and cornelian cherry juices ameliorate metabolic syndrome induced by a high-fat high-fructose diet in Wistar rats",
number = "7",
volume = "10",
doi = "10.1016/j.heliyon.2024.e27709",
pages = "e27709"
}

Paunović, M., Milošević, M., Mitrović-Ajtić, O., Veličković, N., Mićić, B., Nedić, O., Todorović, V., Vučić, V.,& Petrović, S.. (2024). Polyphenol-rich black currant and cornelian cherry juices ameliorate metabolic syndrome induced by a high-fat high-fructose diet in Wistar rats. in Heliyon
Elsevier Ltd.., 10(7), e27709.
https://doi.org/10.1016/j.heliyon.2024.e27709

Paunović M, Milošević M, Mitrović-Ajtić O, Veličković N, Mićić B, Nedić O, Todorović V, Vučić V, Petrović S. Polyphenol-rich black currant and cornelian cherry juices ameliorate metabolic syndrome induced by a high-fat high-fructose diet in Wistar rats. in Heliyon. 2024;10(7):e27709.
doi:10.1016/j.heliyon.2024.e27709 .

Paunović, Marija, Milošević, Maja, Mitrović-Ajtić, Olivera, Veličković, Nataša, Mićić, Bojana, Nedić, Olgica, Todorović, Vanja, Vučić, Vesna, Petrović, Snježana, "Polyphenol-rich black currant and cornelian cherry juices ameliorate metabolic syndrome induced by a high-fat high-fructose diet in Wistar rats" in Heliyon, 10, no. 7 (2024):e27709,
https://doi.org/10.1016/j.heliyon.2024.e27709 . .

TY  - CONF
AU  - Petrović, Snježana
AU  - Paunović, Marija
AU  - Veličković, Nataša
AU  - Mićić, Bojana
AU  - Milošević, Maja
AU  - Arsić, Aleksandra
AU  - Pokimica, Biljana
AU  - Vučić, Vesna
PY  - 2024
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6683
AB  - Our study was aimed to investigate the effects of commercially available, cold-pressed polyphenol-rich black currant (BC) juice on fat accumulation, blood lipids, insulin resistance, high blood pressure, and inflammation, in rats placed on high-fat high-fructose (HFF) diet. Coadministration of BC juice significantly reduced diet-induced adiposity and plasma triglycerides levels, improved glucose tolerance, and suppressed hepatic inflammation during prolonged HFF feeding in rats. These findings suggest that consumption of BC juice may  counter the harmful effects of the Western diet rich in fats and sugars, and to be useful for the prevention of metabolic syndrome development and progression.
PB  - Čačak: Faculty of Agronomy in Čačak, University of Kragujevac
C3  - Proceedings: 2nd International Symposium on Biotechnology: SYMBIOTECH; 2024 Mar 14–15; Čačak, Serbia
T1  - Polyphenol-rich black currant juice ameliorates metabolic syndrome induced by high-fat diet in rats
SP  - 595
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6683
ER  - 

@conference{
author = "Petrović, Snježana and Paunović, Marija and Veličković, Nataša and Mićić, Bojana and Milošević, Maja and Arsić, Aleksandra and Pokimica, Biljana and Vučić, Vesna",
year = "2024",
abstract = "Our study was aimed to investigate the effects of commercially available, cold-pressed polyphenol-rich black currant (BC) juice on fat accumulation, blood lipids, insulin resistance, high blood pressure, and inflammation, in rats placed on high-fat high-fructose (HFF) diet. Coadministration of BC juice significantly reduced diet-induced adiposity and plasma triglycerides levels, improved glucose tolerance, and suppressed hepatic inflammation during prolonged HFF feeding in rats. These findings suggest that consumption of BC juice may  counter the harmful effects of the Western diet rich in fats and sugars, and to be useful for the prevention of metabolic syndrome development and progression.",
publisher = "Čačak: Faculty of Agronomy in Čačak, University of Kragujevac",
journal = "Proceedings: 2nd International Symposium on Biotechnology: SYMBIOTECH; 2024 Mar 14–15; Čačak, Serbia",
title = "Polyphenol-rich black currant juice ameliorates metabolic syndrome induced by high-fat diet in rats",
pages = "595",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6683"
}

Petrović, S., Paunović, M., Veličković, N., Mićić, B., Milošević, M., Arsić, A., Pokimica, B.,& Vučić, V.. (2024). Polyphenol-rich black currant juice ameliorates metabolic syndrome induced by high-fat diet in rats. in Proceedings: 2nd International Symposium on Biotechnology: SYMBIOTECH; 2024 Mar 14–15; Čačak, Serbia
Čačak: Faculty of Agronomy in Čačak, University of Kragujevac., 595.
https://hdl.handle.net/21.15107/rcub_ibiss_6683

Petrović S, Paunović M, Veličković N, Mićić B, Milošević M, Arsić A, Pokimica B, Vučić V. Polyphenol-rich black currant juice ameliorates metabolic syndrome induced by high-fat diet in rats. in Proceedings: 2nd International Symposium on Biotechnology: SYMBIOTECH; 2024 Mar 14–15; Čačak, Serbia. 2024;:595.
https://hdl.handle.net/21.15107/rcub_ibiss_6683 .

Petrović, Snježana, Paunović, Marija, Veličković, Nataša, Mićić, Bojana, Milošević, Maja, Arsić, Aleksandra, Pokimica, Biljana, Vučić, Vesna, "Polyphenol-rich black currant juice ameliorates metabolic syndrome induced by high-fat diet in rats" in Proceedings: 2nd International Symposium on Biotechnology: SYMBIOTECH; 2024 Mar 14–15; Čačak, Serbia (2024):595,
https://hdl.handle.net/21.15107/rcub_ibiss_6683 .

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  - Mićić, Bojana
AU  - Veličković, Nataša
AU  - Đorđević, Ana
AU  - Teofilović, Ana
AU  - Kovačević, Sanja
AU  - Radovanović, Marina
AU  - Brkljačić, Jelena
AU  - Macut Djuro
AU  - Vojnović Milutinović, Danijela
PY  - 2023
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6418
AB  - Introduction: Polycystic ovary syndrome (PCOS) is a common endocrine disorder that affects women’s
fertility and metabolic health throughout their life time. Insulin resistance and obesity, in conjunction
with excess androgens, are undeniably involved in its development. We aimed to elucidate how hyperandrogenemia
and prepubertal adiposity contribute to the development of metabolic disturbances in
rat model of PCOS.
Methods: The animal model of PCOS induced by 5a-dihydrotestosterone (DHT) was additionally challenged
by litter size reduction (LSR) during suckling period, to ensure overfeeding and development of
prepubertal adiposity. Systemic parameters of insulin sensitivity, along with markers of energy sensing,
insulin signaling, and lipid metabolism were analyzed in visceral adipose tissue (VAT) and skeletal muscle.
Results: The combination of treatments led to hyperinsulinemia and impaired systemic insulin sensitivity.
This was not accompanied with altered insulin signaling in the VAT, in spite of observed adipocytes
hypertrophy probably due to activation of AMPK and restrained lipogenesis in this tissue. On the other
hand, insulin signaling in skeletal muscle was impaired, which resulted in increased muscle fatty acid
uptake and oxidation after combined treatment. The switch to fatty acids oxidation subsequently led to
oxidative stress and inflammation, which was followed by adaptive activation of AMPK and increased
expression of its targets involved in antioxidant protection and mitochondrial biogenesis.
Conclusion: Our results suggest that prepubertal weight gain predisposes to insulin resistance development
in androgen-excess PCOS. The protective activation of AMPK in VAT and muscle makes it a potential
therapeutic target for insulin-resistant PCOS patients.
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  - Metabolic disturbances in animal model of polycystic ovary syndrome: impact of early postnatal overfeeding
SP  - 144
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6418
ER  - 

@conference{
author = "Mićić, Bojana and Veličković, Nataša and Đorđević, Ana and Teofilović, Ana and Kovačević, Sanja and Radovanović, Marina and Brkljačić, Jelena and Macut Djuro and Vojnović Milutinović, Danijela",
year = "2023",
abstract = "Introduction: Polycystic ovary syndrome (PCOS) is a common endocrine disorder that affects women’s
fertility and metabolic health throughout their life time. Insulin resistance and obesity, in conjunction
with excess androgens, are undeniably involved in its development. We aimed to elucidate how hyperandrogenemia
and prepubertal adiposity contribute to the development of metabolic disturbances in
rat model of PCOS.
Methods: The animal model of PCOS induced by 5a-dihydrotestosterone (DHT) was additionally challenged
by litter size reduction (LSR) during suckling period, to ensure overfeeding and development of
prepubertal adiposity. Systemic parameters of insulin sensitivity, along with markers of energy sensing,
insulin signaling, and lipid metabolism were analyzed in visceral adipose tissue (VAT) and skeletal muscle.
Results: The combination of treatments led to hyperinsulinemia and impaired systemic insulin sensitivity.
This was not accompanied with altered insulin signaling in the VAT, in spite of observed adipocytes
hypertrophy probably due to activation of AMPK and restrained lipogenesis in this tissue. On the other
hand, insulin signaling in skeletal muscle was impaired, which resulted in increased muscle fatty acid
uptake and oxidation after combined treatment. The switch to fatty acids oxidation subsequently led to
oxidative stress and inflammation, which was followed by adaptive activation of AMPK and increased
expression of its targets involved in antioxidant protection and mitochondrial biogenesis.
Conclusion: Our results suggest that prepubertal weight gain predisposes to insulin resistance development
in androgen-excess PCOS. The protective activation of AMPK in VAT and muscle makes it a potential
therapeutic target for insulin-resistant PCOS patients.",
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 = "Metabolic disturbances in animal model of polycystic ovary syndrome: impact of early postnatal overfeeding",
pages = "144",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6418"
}

Mićić, B., Veličković, N., Đorđević, A., Teofilović, A., Kovačević, S., Radovanović, M., Brkljačić, J., Macut Djuro,& Vojnović Milutinović, D.. (2023). Metabolic disturbances in animal model of polycystic ovary syndrome: impact of early postnatal overfeeding. 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., 144.
https://hdl.handle.net/21.15107/rcub_ibiss_6418

Mićić B, Veličković N, Đorđević A, Teofilović A, Kovačević S, Radovanović M, Brkljačić J, Macut Djuro, Vojnović Milutinović D. Metabolic disturbances in animal model of polycystic ovary syndrome: impact of early postnatal overfeeding. in Abstract Book: CoMBoS2 - the Second Congress of Molecular Biologists of Serbia; 2023 Oct 6-8; Belgrade, Serbia. 2023;:144.
https://hdl.handle.net/21.15107/rcub_ibiss_6418 .

Mićić, Bojana, Veličković, Nataša, Đorđević, Ana, Teofilović, Ana, Kovačević, Sanja, Radovanović, Marina, Brkljačić, Jelena, Macut Djuro, Vojnović Milutinović, Danijela, "Metabolic disturbances in animal model of polycystic ovary syndrome: impact of early postnatal overfeeding" in Abstract Book: CoMBoS2 - the Second Congress of Molecular Biologists of Serbia; 2023 Oct 6-8; Belgrade, Serbia (2023):144,
https://hdl.handle.net/21.15107/rcub_ibiss_6418 .

TY  - JOUR
AU  - Mićić, Bojana
AU  - Đorđević, Ana
AU  - Veličković, Nataša
AU  - Kovačević, Sanja
AU  - Martić, Teodora
AU  - Macut, Đuro
AU  - Vojnović-Milutinović, Danijela
PY  - 2023
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5785
AB  - Polycystic ovary syndrome (PCOS) is a common endocrinopathy in women of reproductive
age, often associated with obesity and insulin resistance. Childhood obesity is an important
predisposing factor for the development of PCOS later in life. Being particularly interested in the
interplay between prepubertal obesity and hyperandrogenemia, we investigated the effects of early
postnatal overfeeding, accomplished by reducing litter size during the period of suckling, on energy
sensing and insulin signaling pathways in the gastrocnemius muscle of a rat model of PCOS-induced
by 5 -dihydrotestosterone (DHT). The combination of overfeeding and DHT treatment caused hyperinsulinemia
and decreased systemic insulin sensitivity. Early postnatal overfeeding induced defects
at critical nodes of the insulin signaling pathway in skeletal muscle, which was associated with
reduced glucose uptake in the presence of hyperandrogenemia. In this setting, under a combination
of overfeeding and DHT treatment, skeletal muscle switched to mitochondrial  -oxidation of fatty
acids, resulting in oxidative stress and inflammation that stimulated AMP-activated protein kinase
(AMPK) activity and its downstream targets involved in mitochondrial biogenesis and antioxidant
protection. Overall, a combination of overfeeding and hyperandrogenemia resulted in a prooxidative
and insulin-resistant state in skeletal muscle. This was accompanied by the activation of AMPK,
which could represent a potential therapeutic target in insulin-resistant PCOS patients.
PB  - Basel: MDPI
T2  - Biomedicines
T1  - AMPK Activation as a Protective Mechanism to Restrain Oxidative Stress in the Insulin-Resistant State in Skeletal Muscle of Rat Model of PCOS Subjected to Postnatal Overfeeding
IS  - 6
VL  - 11
DO  - 10.3390/biomedicines11061586
SP  - 1586
ER  - 

@article{
author = "Mićić, Bojana and Đorđević, Ana and Veličković, Nataša and Kovačević, Sanja and Martić, Teodora and Macut, Đuro and Vojnović-Milutinović, Danijela",
year = "2023",
abstract = "Polycystic ovary syndrome (PCOS) is a common endocrinopathy in women of reproductive
age, often associated with obesity and insulin resistance. Childhood obesity is an important
predisposing factor for the development of PCOS later in life. Being particularly interested in the
interplay between prepubertal obesity and hyperandrogenemia, we investigated the effects of early
postnatal overfeeding, accomplished by reducing litter size during the period of suckling, on energy
sensing and insulin signaling pathways in the gastrocnemius muscle of a rat model of PCOS-induced
by 5 -dihydrotestosterone (DHT). The combination of overfeeding and DHT treatment caused hyperinsulinemia
and decreased systemic insulin sensitivity. Early postnatal overfeeding induced defects
at critical nodes of the insulin signaling pathway in skeletal muscle, which was associated with
reduced glucose uptake in the presence of hyperandrogenemia. In this setting, under a combination
of overfeeding and DHT treatment, skeletal muscle switched to mitochondrial  -oxidation of fatty
acids, resulting in oxidative stress and inflammation that stimulated AMP-activated protein kinase
(AMPK) activity and its downstream targets involved in mitochondrial biogenesis and antioxidant
protection. Overall, a combination of overfeeding and hyperandrogenemia resulted in a prooxidative
and insulin-resistant state in skeletal muscle. This was accompanied by the activation of AMPK,
which could represent a potential therapeutic target in insulin-resistant PCOS patients.",
publisher = "Basel: MDPI",
journal = "Biomedicines",
title = "AMPK Activation as a Protective Mechanism to Restrain Oxidative Stress in the Insulin-Resistant State in Skeletal Muscle of Rat Model of PCOS Subjected to Postnatal Overfeeding",
number = "6",
volume = "11",
doi = "10.3390/biomedicines11061586",
pages = "1586"
}

Mićić, B., Đorđević, A., Veličković, N., Kovačević, S., Martić, T., Macut, Đ.,& Vojnović-Milutinović, D.. (2023). AMPK Activation as a Protective Mechanism to Restrain Oxidative Stress in the Insulin-Resistant State in Skeletal Muscle of Rat Model of PCOS Subjected to Postnatal Overfeeding. in Biomedicines
Basel: MDPI., 11(6), 1586.
https://doi.org/10.3390/biomedicines11061586

Mićić B, Đorđević A, Veličković N, Kovačević S, Martić T, Macut Đ, Vojnović-Milutinović D. AMPK Activation as a Protective Mechanism to Restrain Oxidative Stress in the Insulin-Resistant State in Skeletal Muscle of Rat Model of PCOS Subjected to Postnatal Overfeeding. in Biomedicines. 2023;11(6):1586.
doi:10.3390/biomedicines11061586 .

Mićić, Bojana, Đorđević, Ana, Veličković, Nataša, Kovačević, Sanja, Martić, Teodora, Macut, Đuro, Vojnović-Milutinović, Danijela, "AMPK Activation as a Protective Mechanism to Restrain Oxidative Stress in the Insulin-Resistant State in Skeletal Muscle of Rat Model of PCOS Subjected to Postnatal Overfeeding" in Biomedicines, 11, no. 6 (2023):1586,
https://doi.org/10.3390/biomedicines11061586 . .

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  - Mićić, Bojana
AU  - Teofilović, Ana
AU  - Đorđević, Ana
AU  - Veličković, Nataša
AU  - Macut, Djuro
AU  - Vojnović-Milutinović, Danijela
PY  - 2022
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5022
AB  - Polycystic ovary syndrome (PCOS) is a well-known reproductive syndrome usually associated
with obesity, insulin resistance, and hyperinsulinemia. Although the first signs of PCOS
begin early in adolescence, it is underexplored whether peripubertal obesity predisposes women to
PCOS metabolic disturbances. To highlight that, we examined the impact of postnatal overfeedinginduced
obesity, achieved by litter size reduction during the suckling period, on metabolic disturbances
associated with visceral and subcutaneous adipose tissue (VAT and SAT) function in the
5 -dihydrotestosterone (5 -DHT)-induced animal model of PCOS. We analyzed markers of insulin
signaling, lipid metabolism, and energy sensing in the VAT and SAT. Our results showed that postnatally
overfed DHT-treated Wistar rats had increased VAT mass with hypertrophic adipocytes,
together with hyperinsulinemia and increased HOMA index. In the VAT of these animals, insulin
signaling remained unchanged while lipogenic markers decreased, which was accompanied by
increased AMPK activation. In the SAT of the same animals, markers of lipogenesis and lipolysis
increased, while the activity of AMPK decreased. Taken together, obtained results showed that
postnatal overfeeding predisposes development of PCOS systemic insulin resistance, most likely as
a result of worsened metabolic function of SAT, while VAT preserved its tissue insulin sensitivity
through increased activity of AMPK.
PB  - Basel: MDPI
T2  - International Journal of Molecular Sciences
T1  - AMPK Activation Is Important for the Preservation of Insulin Sensitivity in Visceral, but Not in Subcutaneous Adipose Tissue of Postnatally Overfed Rat Model of Polycystic Ovary Syndrome
IS  - 16
VL  - 23
DO  - 10.3390/ijms23168942
SP  - 8942
ER  - 

@article{
author = "Mićić, Bojana and Teofilović, Ana and Đorđević, Ana and Veličković, Nataša and Macut, Djuro and Vojnović-Milutinović, Danijela",
year = "2022",
abstract = "Polycystic ovary syndrome (PCOS) is a well-known reproductive syndrome usually associated
with obesity, insulin resistance, and hyperinsulinemia. Although the first signs of PCOS
begin early in adolescence, it is underexplored whether peripubertal obesity predisposes women to
PCOS metabolic disturbances. To highlight that, we examined the impact of postnatal overfeedinginduced
obesity, achieved by litter size reduction during the suckling period, on metabolic disturbances
associated with visceral and subcutaneous adipose tissue (VAT and SAT) function in the
5 -dihydrotestosterone (5 -DHT)-induced animal model of PCOS. We analyzed markers of insulin
signaling, lipid metabolism, and energy sensing in the VAT and SAT. Our results showed that postnatally
overfed DHT-treated Wistar rats had increased VAT mass with hypertrophic adipocytes,
together with hyperinsulinemia and increased HOMA index. In the VAT of these animals, insulin
signaling remained unchanged while lipogenic markers decreased, which was accompanied by
increased AMPK activation. In the SAT of the same animals, markers of lipogenesis and lipolysis
increased, while the activity of AMPK decreased. Taken together, obtained results showed that
postnatal overfeeding predisposes development of PCOS systemic insulin resistance, most likely as
a result of worsened metabolic function of SAT, while VAT preserved its tissue insulin sensitivity
through increased activity of AMPK.",
publisher = "Basel: MDPI",
journal = "International Journal of Molecular Sciences",
title = "AMPK Activation Is Important for the Preservation of Insulin Sensitivity in Visceral, but Not in Subcutaneous Adipose Tissue of Postnatally Overfed Rat Model of Polycystic Ovary Syndrome",
number = "16",
volume = "23",
doi = "10.3390/ijms23168942",
pages = "8942"
}

Mićić, B., Teofilović, A., Đorđević, A., Veličković, N., Macut, D.,& Vojnović-Milutinović, D.. (2022). AMPK Activation Is Important for the Preservation of Insulin Sensitivity in Visceral, but Not in Subcutaneous Adipose Tissue of Postnatally Overfed Rat Model of Polycystic Ovary Syndrome. in International Journal of Molecular Sciences
Basel: MDPI., 23(16), 8942.
https://doi.org/10.3390/ijms23168942

Mićić B, Teofilović A, Đorđević A, Veličković N, Macut D, Vojnović-Milutinović D. AMPK Activation Is Important for the Preservation of Insulin Sensitivity in Visceral, but Not in Subcutaneous Adipose Tissue of Postnatally Overfed Rat Model of Polycystic Ovary Syndrome. in International Journal of Molecular Sciences. 2022;23(16):8942.
doi:10.3390/ijms23168942 .

Mićić, Bojana, Teofilović, Ana, Đorđević, Ana, Veličković, Nataša, Macut, Djuro, Vojnović-Milutinović, Danijela, "AMPK Activation Is Important for the Preservation of Insulin Sensitivity in Visceral, but Not in Subcutaneous Adipose Tissue of Postnatally Overfed Rat Model of Polycystic Ovary Syndrome" in International Journal of Molecular Sciences, 23, no. 16 (2022):8942,
https://doi.org/10.3390/ijms23168942 . .

TY  - JOUR
AU  - Teofilović, Ana
AU  - Vratarić, Miloš
AU  - Veličković, Nataša
AU  - Vojnović-Milutinović, Danijela
AU  - Mladenović, Aleksandra
AU  - Prvulović, Milica
AU  - Đorđević, Ana
PY  - 2022
UR  - https://www.frontiersin.org/articles/10.3389/fnut.2022.899255/full
UR  - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC9168317
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5004
AB  - Aging is a progressive process that could disturb metabolic homeostasis in the liver via ectopic lipid accumulation, oxidative stress, and deterioration of inflammatory response. Although calorie restriction (CR) is recognized as beneficial for life span and health span prolongation, it is still unclear how late-onset CR, characterized by late beginning and short duration, affects age-related processes. The aim of this study was to examine how late-onset CR-induced metabolic adjustments impact lipid status and inflammation in the liver of old rats. The experiments were conducted on aging male Wistar rats fed ad libitum (AL) or exposed to late-onset CR (60% of AL daily intake) from 21st to 24th month. The results showed that late-onset CR reduces body weight, visceral adipose tissue and liver mass, and triglyceride levels when compared to old animals on AL diet. The ameliorating effects of CR on lipid metabolism include increased activity of AMP-activated protein kinase, suppressed de novo fatty acid synthesis, stimulated β-oxidation, decreased lipotoxicity, and limited triglyceride synthesis and packaging in the liver. Restricted diet regime, however, does not improve expression of antioxidant enzymes, although it leads to progression of age-related inflammation in the liver, partially through lower corticosterone concentration and decreased activation of glucocorticoid receptor. In conclusion, late-onset CR is able to restore age-related imbalance of lipid metabolism in the liver, but has a negative impact on hepatic inflammatory status, implying that the type of diet for older individuals must be balanced and chosen carefully with appropriate duration and start point.
T2  - Frontiers in Nutrition
T1  - Late-Onset Calorie Restriction Improves Lipid Metabolism and Aggravates Inflammation in the Liver of Old Wistar Rats.
VL  - 9
DO  - 10.3389/fnut.2022.899255
SP  - 899255
ER  - 

@article{
author = "Teofilović, Ana and Vratarić, Miloš and Veličković, Nataša and Vojnović-Milutinović, Danijela and Mladenović, Aleksandra and Prvulović, Milica and Đorđević, Ana",
year = "2022",
abstract = "Aging is a progressive process that could disturb metabolic homeostasis in the liver via ectopic lipid accumulation, oxidative stress, and deterioration of inflammatory response. Although calorie restriction (CR) is recognized as beneficial for life span and health span prolongation, it is still unclear how late-onset CR, characterized by late beginning and short duration, affects age-related processes. The aim of this study was to examine how late-onset CR-induced metabolic adjustments impact lipid status and inflammation in the liver of old rats. The experiments were conducted on aging male Wistar rats fed ad libitum (AL) or exposed to late-onset CR (60% of AL daily intake) from 21st to 24th month. The results showed that late-onset CR reduces body weight, visceral adipose tissue and liver mass, and triglyceride levels when compared to old animals on AL diet. The ameliorating effects of CR on lipid metabolism include increased activity of AMP-activated protein kinase, suppressed de novo fatty acid synthesis, stimulated β-oxidation, decreased lipotoxicity, and limited triglyceride synthesis and packaging in the liver. Restricted diet regime, however, does not improve expression of antioxidant enzymes, although it leads to progression of age-related inflammation in the liver, partially through lower corticosterone concentration and decreased activation of glucocorticoid receptor. In conclusion, late-onset CR is able to restore age-related imbalance of lipid metabolism in the liver, but has a negative impact on hepatic inflammatory status, implying that the type of diet for older individuals must be balanced and chosen carefully with appropriate duration and start point.",
journal = "Frontiers in Nutrition",
title = "Late-Onset Calorie Restriction Improves Lipid Metabolism and Aggravates Inflammation in the Liver of Old Wistar Rats.",
volume = "9",
doi = "10.3389/fnut.2022.899255",
pages = "899255"
}

Teofilović, A., Vratarić, M., Veličković, N., Vojnović-Milutinović, D., Mladenović, A., Prvulović, M.,& Đorđević, A.. (2022). Late-Onset Calorie Restriction Improves Lipid Metabolism and Aggravates Inflammation in the Liver of Old Wistar Rats.. in Frontiers in Nutrition, 9, 899255.
https://doi.org/10.3389/fnut.2022.899255

Teofilović A, Vratarić M, Veličković N, Vojnović-Milutinović D, Mladenović A, Prvulović M, Đorđević A. Late-Onset Calorie Restriction Improves Lipid Metabolism and Aggravates Inflammation in the Liver of Old Wistar Rats.. in Frontiers in Nutrition. 2022;9:899255.
doi:10.3389/fnut.2022.899255 .

Teofilović, Ana, Vratarić, Miloš, Veličković, Nataša, Vojnović-Milutinović, Danijela, Mladenović, Aleksandra, Prvulović, Milica, Đorđević, Ana, "Late-Onset Calorie Restriction Improves Lipid Metabolism and Aggravates Inflammation in the Liver of Old Wistar Rats." in Frontiers in Nutrition, 9 (2022):899255,
https://doi.org/10.3389/fnut.2022.899255 . .

TY  - JOUR
AU  - Vojnović-Milutinović, Danijela
AU  - Teofilović, Ana
AU  - Veličković, Nataša
AU  - Brkljačić, Jelena
AU  - Jelača, Sanja
AU  - Đorđević, Ana
AU  - Macut, Đuro
PY  - 2021
UR  - https://doi.org/10.1007/s12020-020-02600-1
UR  - http://www.ncbi.nlm.nih.gov/pubmed/33449293
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4146
AB  - PURPOSE Polycystic ovary syndrome (PCOS) is a complex reproductive disorder often associated with obesity, insulin resistance, and dyslipidemia. Hormonal changes in PCOS may also include altered glucocorticoid signaling. Our aim was to examine whether alterations in hepatic glucocorticoid signaling are associated with disturbances of glucose and lipid metabolism in animal model of PCOS. METHODS Female rats, 3 weeks old, were subcutaneously implanted with 5α-dihydrotestosterone (DHT) or placebo pellets for 90 days to induce PCOS. Expression of 11β-hydroxysteroid dehydrogenase 1 (11βHSD1) and A-ring reductases (5α and 5β), as well as intracellular distribution of glucocorticoid receptor (GR) and expression of its regulated genes were examined in the liver. Proteins of hepatic lipid and carbohydrate metabolism and markers of inflammation were also assessed. RESULTS DHT treatment induced increase in body and liver mass, as well as in triglycerides and free fatty acids levels in plasma. Elevation of 11βHSD1 and reduction of 5α-reductase expression was observed together with increased hepatic corticosterone concentration and nuclear GR activation. Induced expression of Krüppel-like factor 15 and decreased expression of genes for proinflammatory cytokines and de novo lipogenesis (DNL) were detected in the liver of DHT-treated rats, while DNL regulators and proinflammatory markers were not changed. However, increased mRNA levels of stearoyl-CoA desaturase and apolipoprotein B were observed in DHT animals. CONCLUSIONS DHT treatment stimulated hepatic glucocorticoid prereceptor metabolism through increased corticosterone availability which is associated with enhanced GR activation. This does not affect gluconeogenesis and DNL, but could be linked to stimulated triglyceride synthesis and hypertriglyceridemia.
PB  - Springer
T2  - Endocrine
T1  - Glucocorticoid signaling and lipid metabolism disturbances in the liver of rats treated with 5α-dihydrotestosterone in an animal model of polycystic ovary syndrome.
DO  - 10.1007/s12020-020-02600-1
ER  - 

@article{
author = "Vojnović-Milutinović, Danijela and Teofilović, Ana and Veličković, Nataša and Brkljačić, Jelena and Jelača, Sanja and Đorđević, Ana and Macut, Đuro",
year = "2021",
abstract = "PURPOSE Polycystic ovary syndrome (PCOS) is a complex reproductive disorder often associated with obesity, insulin resistance, and dyslipidemia. Hormonal changes in PCOS may also include altered glucocorticoid signaling. Our aim was to examine whether alterations in hepatic glucocorticoid signaling are associated with disturbances of glucose and lipid metabolism in animal model of PCOS. METHODS Female rats, 3 weeks old, were subcutaneously implanted with 5α-dihydrotestosterone (DHT) or placebo pellets for 90 days to induce PCOS. Expression of 11β-hydroxysteroid dehydrogenase 1 (11βHSD1) and A-ring reductases (5α and 5β), as well as intracellular distribution of glucocorticoid receptor (GR) and expression of its regulated genes were examined in the liver. Proteins of hepatic lipid and carbohydrate metabolism and markers of inflammation were also assessed. RESULTS DHT treatment induced increase in body and liver mass, as well as in triglycerides and free fatty acids levels in plasma. Elevation of 11βHSD1 and reduction of 5α-reductase expression was observed together with increased hepatic corticosterone concentration and nuclear GR activation. Induced expression of Krüppel-like factor 15 and decreased expression of genes for proinflammatory cytokines and de novo lipogenesis (DNL) were detected in the liver of DHT-treated rats, while DNL regulators and proinflammatory markers were not changed. However, increased mRNA levels of stearoyl-CoA desaturase and apolipoprotein B were observed in DHT animals. CONCLUSIONS DHT treatment stimulated hepatic glucocorticoid prereceptor metabolism through increased corticosterone availability which is associated with enhanced GR activation. This does not affect gluconeogenesis and DNL, but could be linked to stimulated triglyceride synthesis and hypertriglyceridemia.",
publisher = "Springer",
journal = "Endocrine",
title = "Glucocorticoid signaling and lipid metabolism disturbances in the liver of rats treated with 5α-dihydrotestosterone in an animal model of polycystic ovary syndrome.",
doi = "10.1007/s12020-020-02600-1"
}

Vojnović-Milutinović, D., Teofilović, A., Veličković, N., Brkljačić, J., Jelača, S., Đorđević, A.,& Macut, Đ.. (2021). Glucocorticoid signaling and lipid metabolism disturbances in the liver of rats treated with 5α-dihydrotestosterone in an animal model of polycystic ovary syndrome.. in Endocrine
Springer..
https://doi.org/10.1007/s12020-020-02600-1

Vojnović-Milutinović D, Teofilović A, Veličković N, Brkljačić J, Jelača S, Đorđević A, Macut Đ. Glucocorticoid signaling and lipid metabolism disturbances in the liver of rats treated with 5α-dihydrotestosterone in an animal model of polycystic ovary syndrome.. in Endocrine. 2021;.
doi:10.1007/s12020-020-02600-1 .

Vojnović-Milutinović, Danijela, Teofilović, Ana, Veličković, Nataša, Brkljačić, Jelena, Jelača, Sanja, Đorđević, Ana, Macut, Đuro, "Glucocorticoid signaling and lipid metabolism disturbances in the liver of rats treated with 5α-dihydrotestosterone in an animal model of polycystic ovary syndrome." in Endocrine (2021),
https://doi.org/10.1007/s12020-020-02600-1 . .

TY  - JOUR
AU  - Gligorovska, Ljupka
AU  - Teofilović, Ana
AU  - Vojnović-Milutinović, Danijela
AU  - Miladinović, Nenad
AU  - Kovačević, Sanja
AU  - Veličković, Nataša
AU  - Đorđević, Ana
PY  - 2021
UR  - https://onlinelibrary.wiley.com/doi/10.1002/biof.1711
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4148
AB  - Dietary fructose can disturb hepatic lipid metabolism in a way that leads to lipid accumulation and steatosis, which is often accompanied with low-grade inflammation. The macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine with important role not only in the regulation of inflammation, but also in the modulation of energy metabolism in the liver. Thus, the aim of this study was to investigate the role of Mif deficiency in fructose-induced disturbances of hepatic lipid metabolism and ectopic lipid accumulation. Wild type (WT) and Mif deficient (MIF−/−) C57Bl/6J mice were used to analyze the effects of 9-week 20% fructose-enriched diet on hepatic lipid metabolism (both lipogenesis and β-oxidation) and histology, inflammatory status and glucocorticoid receptor (GR) signaling. The results showed fructose-induced elevation of lipogenic genes (fatty acid synthase (Fas) and stearoyl-CoA desaturase-1 (Scd1) and transcriptional lipogenic regulators (liver X receptor (LXR), sterol regulatory element binding protein 1c (SREBP1c), and carbohydrate response element-binding protein (ChREBP)). However, microvesicular fatty changes, accompanied with enhanced inflammation, were observable only in fructose-fed Mif deficient animals, and were most likely result of GR activation and facilitated uptake and decreased β-oxidation of FFA, as evidenced by elevated protein level of fatty acid translocase (FAT/CD36) and decreased carnitine palmitoyl transferase 1 (CPT1) level. In conclusion, the results show that Mif deficiency aggravates the effects of energy-rich fructose diet on hepatic lipid accumulation, most likely through enhanced inflammation and activation of GR signaling pathway.
PB  - Blackwell Publishing Inc.
T2  - BioFactors
T1  - Macrophage migration inhibitory factor deficiency aggravates effects of fructose‐enriched diet on lipid metabolism in the mouse liver
DO  - 10.1002/biof.1711
SP  - biof.1711
ER  - 

@article{
author = "Gligorovska, Ljupka and Teofilović, Ana and Vojnović-Milutinović, Danijela and Miladinović, Nenad and Kovačević, Sanja and Veličković, Nataša and Đorđević, Ana",
year = "2021",
abstract = "Dietary fructose can disturb hepatic lipid metabolism in a way that leads to lipid accumulation and steatosis, which is often accompanied with low-grade inflammation. The macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine with important role not only in the regulation of inflammation, but also in the modulation of energy metabolism in the liver. Thus, the aim of this study was to investigate the role of Mif deficiency in fructose-induced disturbances of hepatic lipid metabolism and ectopic lipid accumulation. Wild type (WT) and Mif deficient (MIF−/−) C57Bl/6J mice were used to analyze the effects of 9-week 20% fructose-enriched diet on hepatic lipid metabolism (both lipogenesis and β-oxidation) and histology, inflammatory status and glucocorticoid receptor (GR) signaling. The results showed fructose-induced elevation of lipogenic genes (fatty acid synthase (Fas) and stearoyl-CoA desaturase-1 (Scd1) and transcriptional lipogenic regulators (liver X receptor (LXR), sterol regulatory element binding protein 1c (SREBP1c), and carbohydrate response element-binding protein (ChREBP)). However, microvesicular fatty changes, accompanied with enhanced inflammation, were observable only in fructose-fed Mif deficient animals, and were most likely result of GR activation and facilitated uptake and decreased β-oxidation of FFA, as evidenced by elevated protein level of fatty acid translocase (FAT/CD36) and decreased carnitine palmitoyl transferase 1 (CPT1) level. In conclusion, the results show that Mif deficiency aggravates the effects of energy-rich fructose diet on hepatic lipid accumulation, most likely through enhanced inflammation and activation of GR signaling pathway.",
publisher = "Blackwell Publishing Inc.",
journal = "BioFactors",
title = "Macrophage migration inhibitory factor deficiency aggravates effects of fructose‐enriched diet on lipid metabolism in the mouse liver",
doi = "10.1002/biof.1711",
pages = "biof.1711"
}

Gligorovska, L., Teofilović, A., Vojnović-Milutinović, D., Miladinović, N., Kovačević, S., Veličković, N.,& Đorđević, A.. (2021). Macrophage migration inhibitory factor deficiency aggravates effects of fructose‐enriched diet on lipid metabolism in the mouse liver. in BioFactors
Blackwell Publishing Inc.., biof.1711.
https://doi.org/10.1002/biof.1711

Gligorovska L, Teofilović A, Vojnović-Milutinović D, Miladinović N, Kovačević S, Veličković N, Đorđević A. Macrophage migration inhibitory factor deficiency aggravates effects of fructose‐enriched diet on lipid metabolism in the mouse liver. in BioFactors. 2021;:biof.1711.
doi:10.1002/biof.1711 .

Gligorovska, Ljupka, Teofilović, Ana, Vojnović-Milutinović, Danijela, Miladinović, Nenad, Kovačević, Sanja, Veličković, Nataša, Đorđević, Ana, "Macrophage migration inhibitory factor deficiency aggravates effects of fructose‐enriched diet on lipid metabolism in the mouse liver" in BioFactors (2021):biof.1711,
https://doi.org/10.1002/biof.1711 . .

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  - 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  - CONF
AU  - Teofilović, Ana
AU  - Vratarić, Miloš
AU  - Veličković, Nataša
AU  - Vojnović-Milutinović, Danijela
AU  - Prvulović, Milica
AU  - Todorović, Smilja
AU  - Mladenović, Aleksandra
AU  - Đorđević, Ana
PY  - 2021
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4281
AB  - Objectives: Dietary restriction (DR) is the approach often used
to delay the development of age-related disorders. One of the unresolved
questions is how late beginning and short duration of DR
affects disturbed metabolic balance caused by ageing. Glucocorticoid
hormones have significant role in the regulation of energy metabolism
and inflammation, especially during ageing when their
systemic
concentration arise. The aim of this study was to examine
the impact of glucocorticoid signaling alterations induced by the
late-onset DR on metabolic inflammation in the liver of old Wistar
rats.
Methods: The experiments were conducted on 6- and
24‑month‑old male Wistar rats on ad libitum diet and
24‑month‑old animals on restrictive diet (60% of ad libitum daily
intake) from 21st to 24th month (late-onset DR). The gene expression
of proinflammatory cytokines was measured by qPCR, while
protein levels of nuclear factor κB (NFκB) and antioxidant enzymes
were determined by Western blot. Glucocorticoid signaling was
analyzed at the level of glucocorticoid prereceptor metabolism and
subcellular distribution of glucocorticoid receptor (GR). Liver corticosterone
concentration was measured by ELISA.
Results: Decreased levels of antioxidant enzymes observed
during ageing were accompanied with augmented inflammation,
characterized by increased nuclear NFκB protein level and higher
expression of Toll like receptor 4 and TNFα. Corticosterone concentration
in the liver of old rats was increased despite unchanged
level of proteins involved in glucocorticoid prereceptor metabolism.
Late-onset DR reduced adipose tissue and liver mass of old
animals, and further stimulated inflammation in the liver.
Decreased level of hepatic corticosterone after DR was a consequence
of increased expression of 5α-reductase which was in
agreement with the decreased GR protein level in the nuclear
fraction.
Conclusion: Late-onset DR did not improve expression of antioxidant
enzymes and led to progression of age-related inflammation
in the liver. This was accompanied with decreased levels of
corticosterone and GR in the nucleus implying that late-onset DR
aggravates inflammatory response through decreased glucocorticoid
signaling in the liver of old rats.
PB  - Basel: S Karger AG
C3  - Proceedings from the 4th European Summer School on Nutrigenomics; 2021 Jun 21-25; Online
T1  - Glucocorticoid Signaling Alterations Induced by Late-Onset Dietary Resctriction Aggravate Metabolic Inflammation in the Liver of Old Wistar Rats
DO  - https://doi.org/10.1159/000517609
SP  - 13
ER  - 

@conference{
author = "Teofilović, Ana and Vratarić, Miloš and Veličković, Nataša and Vojnović-Milutinović, Danijela and Prvulović, Milica and Todorović, Smilja and Mladenović, Aleksandra and Đorđević, Ana",
year = "2021",
abstract = "Objectives: Dietary restriction (DR) is the approach often used
to delay the development of age-related disorders. One of the unresolved
questions is how late beginning and short duration of DR
affects disturbed metabolic balance caused by ageing. Glucocorticoid
hormones have significant role in the regulation of energy metabolism
and inflammation, especially during ageing when their
systemic
concentration arise. The aim of this study was to examine
the impact of glucocorticoid signaling alterations induced by the
late-onset DR on metabolic inflammation in the liver of old Wistar
rats.
Methods: The experiments were conducted on 6- and
24‑month‑old male Wistar rats on ad libitum diet and
24‑month‑old animals on restrictive diet (60% of ad libitum daily
intake) from 21st to 24th month (late-onset DR). The gene expression
of proinflammatory cytokines was measured by qPCR, while
protein levels of nuclear factor κB (NFκB) and antioxidant enzymes
were determined by Western blot. Glucocorticoid signaling was
analyzed at the level of glucocorticoid prereceptor metabolism and
subcellular distribution of glucocorticoid receptor (GR). Liver corticosterone
concentration was measured by ELISA.
Results: Decreased levels of antioxidant enzymes observed
during ageing were accompanied with augmented inflammation,
characterized by increased nuclear NFκB protein level and higher
expression of Toll like receptor 4 and TNFα. Corticosterone concentration
in the liver of old rats was increased despite unchanged
level of proteins involved in glucocorticoid prereceptor metabolism.
Late-onset DR reduced adipose tissue and liver mass of old
animals, and further stimulated inflammation in the liver.
Decreased level of hepatic corticosterone after DR was a consequence
of increased expression of 5α-reductase which was in
agreement with the decreased GR protein level in the nuclear
fraction.
Conclusion: Late-onset DR did not improve expression of antioxidant
enzymes and led to progression of age-related inflammation
in the liver. This was accompanied with decreased levels of
corticosterone and GR in the nucleus implying that late-onset DR
aggravates inflammatory response through decreased glucocorticoid
signaling in the liver of old rats.",
publisher = "Basel: S Karger AG",
journal = "Proceedings from the 4th European Summer School on Nutrigenomics; 2021 Jun 21-25; Online",
title = "Glucocorticoid Signaling Alterations Induced by Late-Onset Dietary Resctriction Aggravate Metabolic Inflammation in the Liver of Old Wistar Rats",
doi = "https://doi.org/10.1159/000517609",
pages = "13"
}

Teofilović, A., Vratarić, M., Veličković, N., Vojnović-Milutinović, D., Prvulović, M., Todorović, S., Mladenović, A.,& Đorđević, A.. (2021). Glucocorticoid Signaling Alterations Induced by Late-Onset Dietary Resctriction Aggravate Metabolic Inflammation in the Liver of Old Wistar Rats. in Proceedings from the 4th European Summer School on Nutrigenomics; 2021 Jun 21-25; Online
Basel: S Karger AG., 13.
https://doi.org/https://doi.org/10.1159/000517609

Teofilović A, Vratarić M, Veličković N, Vojnović-Milutinović D, Prvulović M, Todorović S, Mladenović A, Đorđević A. Glucocorticoid Signaling Alterations Induced by Late-Onset Dietary Resctriction Aggravate Metabolic Inflammation in the Liver of Old Wistar Rats. in Proceedings from the 4th European Summer School on Nutrigenomics; 2021 Jun 21-25; Online. 2021;:13.
doi:https://doi.org/10.1159/000517609 .

Teofilović, Ana, Vratarić, Miloš, Veličković, Nataša, Vojnović-Milutinović, Danijela, Prvulović, Milica, Todorović, Smilja, Mladenović, Aleksandra, Đorđević, Ana, "Glucocorticoid Signaling Alterations Induced by Late-Onset Dietary Resctriction Aggravate Metabolic Inflammation in the Liver of Old Wistar Rats" in Proceedings from the 4th European Summer School on Nutrigenomics; 2021 Jun 21-25; Online (2021):13,
https://doi.org/https://doi.org/10.1159/000517609 . .

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  - Teofilović, Ana
AU  - Brkljačić, Jelena
AU  - Đorđević, Ana
AU  - Vojnović-Milutinović, Danijela
AU  - Tappy, Luc
AU  - Matić, Gordana
AU  - Veličković, Nataša
PY  - 2020
UR  - https://www.tandfonline.com/doi/full/10.1080/09637486.2020.1728236?af=R&utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3615
AB  - Overconsumption of fructose-enriched beverages and everyday stress are involved in the pathogenesis of metabolic disorders through modulation of hepatic glucose metabolism. The aim of the study was to investigate whether interaction of high-fructose diet and chronic stress alter insulin and glucocorticoid signalling thus affecting hepatic glucose homeostasis. High-fructose diet led to hyperinsulinemia, increased glucose transporter 2 level, elevated protein kinase B (Akt) phosphorylation, increased glucokinase mRNA and phospho-to-total glycogen synthase kinase 3 ratio and decreased expression of gluconeogenic genes. Fructose diet also led to stimulated glucocorticoid prereceptor metabolism, but downstream signalling remained unchanged due to increased glucocorticoid clearance. Stress did not affect hepatic insulin and glucocorticoid signalling nor glucose metabolism, while the interaction of the factors was observed only for glucokinase expression. The results suggest that, under conditions of fructose-induced hyperinsulinemia, suppression of gluconeogenesis and glycogen synthase activation contribute to the maintenance of glucose homeostasis. The increased glucocorticoid inactivation may represent an adaptive mechanism to prevent hyperglycaemia.
T2  - International Journal of Food Sciences and Nutrition
T1  - Impact of insulin and glucocorticoid signalling on hepatic glucose homeostasis in the rat exposed to high-fructose diet and chronic stress.
IS  - 7
VL  - 71
DO  - 10.1080/09637486.2020.1728236
SP  - 815
EP  - 825
ER  - 

@article{
author = "Teofilović, Ana and Brkljačić, Jelena and Đorđević, Ana and Vojnović-Milutinović, Danijela and Tappy, Luc and Matić, Gordana and Veličković, Nataša",
year = "2020",
abstract = "Overconsumption of fructose-enriched beverages and everyday stress are involved in the pathogenesis of metabolic disorders through modulation of hepatic glucose metabolism. The aim of the study was to investigate whether interaction of high-fructose diet and chronic stress alter insulin and glucocorticoid signalling thus affecting hepatic glucose homeostasis. High-fructose diet led to hyperinsulinemia, increased glucose transporter 2 level, elevated protein kinase B (Akt) phosphorylation, increased glucokinase mRNA and phospho-to-total glycogen synthase kinase 3 ratio and decreased expression of gluconeogenic genes. Fructose diet also led to stimulated glucocorticoid prereceptor metabolism, but downstream signalling remained unchanged due to increased glucocorticoid clearance. Stress did not affect hepatic insulin and glucocorticoid signalling nor glucose metabolism, while the interaction of the factors was observed only for glucokinase expression. The results suggest that, under conditions of fructose-induced hyperinsulinemia, suppression of gluconeogenesis and glycogen synthase activation contribute to the maintenance of glucose homeostasis. The increased glucocorticoid inactivation may represent an adaptive mechanism to prevent hyperglycaemia.",
journal = "International Journal of Food Sciences and Nutrition",
title = "Impact of insulin and glucocorticoid signalling on hepatic glucose homeostasis in the rat exposed to high-fructose diet and chronic stress.",
number = "7",
volume = "71",
doi = "10.1080/09637486.2020.1728236",
pages = "815-825"
}

Teofilović, A., Brkljačić, J., Đorđević, A., Vojnović-Milutinović, D., Tappy, L., Matić, G.,& Veličković, N.. (2020). Impact of insulin and glucocorticoid signalling on hepatic glucose homeostasis in the rat exposed to high-fructose diet and chronic stress.. in International Journal of Food Sciences and Nutrition, 71(7), 815-825.
https://doi.org/10.1080/09637486.2020.1728236

Teofilović A, Brkljačić J, Đorđević A, Vojnović-Milutinović D, Tappy L, Matić G, Veličković N. Impact of insulin and glucocorticoid signalling on hepatic glucose homeostasis in the rat exposed to high-fructose diet and chronic stress.. in International Journal of Food Sciences and Nutrition. 2020;71(7):815-825.
doi:10.1080/09637486.2020.1728236 .

Teofilović, Ana, Brkljačić, Jelena, Đorđević, Ana, Vojnović-Milutinović, Danijela, Tappy, Luc, Matić, Gordana, Veličković, Nataša, "Impact of insulin and glucocorticoid signalling on hepatic glucose homeostasis in the rat exposed to high-fructose diet and chronic stress." in International Journal of Food Sciences and Nutrition, 71, no. 7 (2020):815-825,
https://doi.org/10.1080/09637486.2020.1728236 . .

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  - Gligorovska, Ljupka
AU  - Teofilović, Ana
AU  - Veličković, Nataša
AU  - Vojnović-Milutinović, Danijela
AU  - Kovačević, Sanja
AU  - Matić, Gordana
AU  - Đorđević, Ana
PY  - 2019
UR  - https://www.faobmbkl2019.com/abstract-book
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3993
AB  - The macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine involved in metabolic inflammation and regulation of energy metabolism in the liver. Genetic deletion of Mif may contribute to the development of systemic insulin resistance, while fructose overload can disturb hepatic lipid metabolism leading to steatosis, inflammation and type 2 diabetes. The aim of the present study was to elucidate the impact of combined effects of Mif deficiency and fructose-enriched diet on insulin sensitivity and lipid metabolism in the liver of male mice. We analysed the effects of 9-week 20 % fructose-enriched diet on indicators of systemic insulin sensitivity, liver histology and biochemical parameters of lipid metabolism in wild type and MIF deficient (MIF−/−) C57Bl/6J mice. The expression of the following lipogenic genes was examined: fatty acid synthase (Fas), acetyl-CoA carboxylase (Acc) and stearoyl-CoA desaturase-1 (Scd1). Levels of insulin-regulated transcriptional factors involved in lipogenesis (sterol regulatory element-binding protein-1c, SREBP-1c and carbohydrate-response element-binding protein, ChREBP), together with the expression of hepatic fatty acid metabolism regulator (peroxisome-proliferator-activated receptor α, PPARα) were also analysed. Mif deficiency did not affect plasma free fatty acid and triglyceride levels, but impaired systemic insulin sensitivity regardless of the diet. In MIF−/− animals, liver histological analysis confirmed the presence of lipid droplets and focal necrosis, but these effects were more pronounced in MIF−/− mice on fructose diet. Although Acc and Fas levels were unchanged, elevated levels of Scd1, SREBP-1c and ChREBP, together with decreased PPARα protein level, were most likely responsible for the lipid accumulation observed in the liver of MIF−/− animals. In conclusion, the results show that energy-rich fructose diet potentiates the effects of Mif deficiency on development of fatty liver and systemic insulin resistance.
PB  - Malaysian Society for Biochemistry and Molecular Biology
PB  - Federation of Asian and Oceanian Biochemists and Molecular Biologists (FAOBMB)
PB  - The International Union of Biochemistry and Molecular Biology (IUBMB)
C3  - Kuala Lumpur, Malaysia : 27th FAOBMB & 44th MSBMB Conference Young Scientist Program (YSP), Abstract Book
T1  - Effects of Mif deficiency and fructose-enriched diet on lipid metabolism in the mouse liver
SP  - 39
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_3993
ER  - 

@conference{
author = "Gligorovska, Ljupka and Teofilović, Ana and Veličković, Nataša and Vojnović-Milutinović, Danijela and Kovačević, Sanja and Matić, Gordana and Đorđević, Ana",
year = "2019",
abstract = "The macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine involved in metabolic inflammation and regulation of energy metabolism in the liver. Genetic deletion of Mif may contribute to the development of systemic insulin resistance, while fructose overload can disturb hepatic lipid metabolism leading to steatosis, inflammation and type 2 diabetes. The aim of the present study was to elucidate the impact of combined effects of Mif deficiency and fructose-enriched diet on insulin sensitivity and lipid metabolism in the liver of male mice. We analysed the effects of 9-week 20 % fructose-enriched diet on indicators of systemic insulin sensitivity, liver histology and biochemical parameters of lipid metabolism in wild type and MIF deficient (MIF−/−) C57Bl/6J mice. The expression of the following lipogenic genes was examined: fatty acid synthase (Fas), acetyl-CoA carboxylase (Acc) and stearoyl-CoA desaturase-1 (Scd1). Levels of insulin-regulated transcriptional factors involved in lipogenesis (sterol regulatory element-binding protein-1c, SREBP-1c and carbohydrate-response element-binding protein, ChREBP), together with the expression of hepatic fatty acid metabolism regulator (peroxisome-proliferator-activated receptor α, PPARα) were also analysed. Mif deficiency did not affect plasma free fatty acid and triglyceride levels, but impaired systemic insulin sensitivity regardless of the diet. In MIF−/− animals, liver histological analysis confirmed the presence of lipid droplets and focal necrosis, but these effects were more pronounced in MIF−/− mice on fructose diet. Although Acc and Fas levels were unchanged, elevated levels of Scd1, SREBP-1c and ChREBP, together with decreased PPARα protein level, were most likely responsible for the lipid accumulation observed in the liver of MIF−/− animals. In conclusion, the results show that energy-rich fructose diet potentiates the effects of Mif deficiency on development of fatty liver and systemic insulin resistance.",
publisher = "Malaysian Society for Biochemistry and Molecular Biology, Federation of Asian and Oceanian Biochemists and Molecular Biologists (FAOBMB), The International Union of Biochemistry and Molecular Biology (IUBMB)",
journal = "Kuala Lumpur, Malaysia : 27th FAOBMB & 44th MSBMB Conference Young Scientist Program (YSP), Abstract Book",
title = "Effects of Mif deficiency and fructose-enriched diet on lipid metabolism in the mouse liver",
pages = "39",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_3993"
}

Gligorovska, L., Teofilović, A., Veličković, N., Vojnović-Milutinović, D., Kovačević, S., Matić, G.,& Đorđević, A.. (2019). Effects of Mif deficiency and fructose-enriched diet on lipid metabolism in the mouse liver. in Kuala Lumpur, Malaysia : 27th FAOBMB & 44th MSBMB Conference Young Scientist Program (YSP), Abstract Book
Malaysian Society for Biochemistry and Molecular Biology., 39.
https://hdl.handle.net/21.15107/rcub_ibiss_3993

Gligorovska L, Teofilović A, Veličković N, Vojnović-Milutinović D, Kovačević S, Matić G, Đorđević A. Effects of Mif deficiency and fructose-enriched diet on lipid metabolism in the mouse liver. in Kuala Lumpur, Malaysia : 27th FAOBMB & 44th MSBMB Conference Young Scientist Program (YSP), Abstract Book. 2019;:39.
https://hdl.handle.net/21.15107/rcub_ibiss_3993 .

Gligorovska, Ljupka, Teofilović, Ana, Veličković, Nataša, Vojnović-Milutinović, Danijela, Kovačević, Sanja, Matić, Gordana, Đorđević, Ana, "Effects of Mif deficiency and fructose-enriched diet on lipid metabolism in the mouse liver" in Kuala Lumpur, Malaysia : 27th FAOBMB & 44th MSBMB Conference Young Scientist Program (YSP), Abstract Book (2019):39,
https://hdl.handle.net/21.15107/rcub_ibiss_3993 .

TY  - CONF
AU  - Gligorovska, Ljupka
AU  - Teofilović, Ana
AU  - Veličković, Nataša
AU  - Vojnović-Milutinović, Danijela
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/123456789/3990
AB  - Introduction: The macrophage migration inhibitory factor (MIF) is a key pro-inflammatory mediator involved in the regulation of energy metabolism and metabolic inflammation in the liver. Fructose overconsumption has been previously associated with development of low-grade inflammation characterized by elevated production of pro-inflammatory cytokines and activation of mitogen-activated protein kinase (MAPK) signaling pathway. The inflammatory response can disrupt insulin signaling and genetic deletion of Mif may contribute to the development of systemic insulin resistance, as well. The aim: The aim of the present study was to elucidate combined effects of Mif deficiency and fructose-enriched diet on metabolic inflammation and insulin sensitivity in the liver of male mice. Methods: Wild type (WT) and Mif deficient (MIF−/−) C57Bl/6J mice were used to analyze the effects of 9-week 20% fructose-enriched diet on indicators of insulin sensitivity and markers of metabolic inflammation (tumor necrosis factor α (TNFα), interleukin (IL)-1β and IL-6). Deregulation of Akt signaling pathway was used as hallmark of hepatic insulin resistance. Also, the protein levels of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase 1 (JNK) and p38 were analyzed. Results: Mif deficient animals exibited elevated expression of IL-1β and IL-6 in the liver, regardless of the diet regime, while hepatic TNFα was unchanged in all animals. On the other hand, both total and phosphorylated ERK and JNK protein levels were decreased in all fructose-fed mice. In the same animals, impaired hepatic insulin signaling, revealed by decreased pAkt and total Akt protein levels, was observed. Conclusion: Although, Mif deficiency led to upregulation of pro-inflammatory cytokines, fructose diet did not aggravate this effect. On the other hand, insulin signalling was diminished by fructose feding independently of Mif deficiency.
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
T1  - Inflammation and Insulin Sensitivity in The Liver of Fructose-fed Mif Deficient Mice
SP  - 53
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_3990
ER  - 

@conference{
author = "Gligorovska, Ljupka and Teofilović, Ana and Veličković, Nataša and Vojnović-Milutinović, Danijela and Kovačević, Sanja and Matić, Gordana and Đorđević, Ana",
year = "2019",
abstract = "Introduction: The macrophage migration inhibitory factor (MIF) is a key pro-inflammatory mediator involved in the regulation of energy metabolism and metabolic inflammation in the liver. Fructose overconsumption has been previously associated with development of low-grade inflammation characterized by elevated production of pro-inflammatory cytokines and activation of mitogen-activated protein kinase (MAPK) signaling pathway. The inflammatory response can disrupt insulin signaling and genetic deletion of Mif may contribute to the development of systemic insulin resistance, as well. The aim: The aim of the present study was to elucidate combined effects of Mif deficiency and fructose-enriched diet on metabolic inflammation and insulin sensitivity in the liver of male mice. Methods: Wild type (WT) and Mif deficient (MIF−/−) C57Bl/6J mice were used to analyze the effects of 9-week 20% fructose-enriched diet on indicators of insulin sensitivity and markers of metabolic inflammation (tumor necrosis factor α (TNFα), interleukin (IL)-1β and IL-6). Deregulation of Akt signaling pathway was used as hallmark of hepatic insulin resistance. Also, the protein levels of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase 1 (JNK) and p38 were analyzed. Results: Mif deficient animals exibited elevated expression of IL-1β and IL-6 in the liver, regardless of the diet regime, while hepatic TNFα was unchanged in all animals. On the other hand, both total and phosphorylated ERK and JNK protein levels were decreased in all fructose-fed mice. In the same animals, impaired hepatic insulin signaling, revealed by decreased pAkt and total Akt protein levels, was observed. Conclusion: Although, Mif deficiency led to upregulation of pro-inflammatory cytokines, fructose diet did not aggravate this effect. On the other hand, insulin signalling was diminished by fructose feding independently of Mif deficiency.",
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",
title = "Inflammation and Insulin Sensitivity in The Liver of Fructose-fed Mif Deficient Mice",
pages = "53",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_3990"
}

Gligorovska, L., Teofilović, A., Veličković, N., Vojnović-Milutinović, D., Kovačević, S., Matić, G.,& Đorđević, A.. (2019). Inflammation and Insulin Sensitivity in The Liver of Fructose-fed Mif Deficient Mice. in Immunology At The Confluence of Multidisciplinary Approaches
Institute for Biological Research "Siniša Stanković" - National Institute of Republic of Serbia, University of Belgrade., 53.
https://hdl.handle.net/21.15107/rcub_ibiss_3990

Gligorovska L, Teofilović A, Veličković N, Vojnović-Milutinović D, Kovačević S, Matić G, Đorđević A. Inflammation and Insulin Sensitivity in The Liver of Fructose-fed Mif Deficient Mice. in Immunology At The Confluence of Multidisciplinary Approaches. 2019;:53.
https://hdl.handle.net/21.15107/rcub_ibiss_3990 .

Gligorovska, Ljupka, Teofilović, Ana, Veličković, Nataša, Vojnović-Milutinović, Danijela, Kovačević, Sanja, Matić, Gordana, Đorđević, Ana, "Inflammation and Insulin Sensitivity in The Liver of Fructose-fed Mif Deficient Mice" in Immunology At The Confluence of Multidisciplinary Approaches (2019):53,
https://hdl.handle.net/21.15107/rcub_ibiss_3990 .

TY  - CHAP
AU  - Đorđević, Ana
AU  - Veličković, Nataša
PY  - 2019
UR  - https://linkinghub.elsevier.com/retrieve/pii/B9780128152607000018
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3963
AB  - Fructose has been a part of human diet for centuries, but in the last 50 years the consumption of fructose-sweetened soft drinks has risen significantly and it was associated with prevalence of obesity and metabolic syndrome. Fructose overconsumption leads to enhanced de novo lipogenesis and triglyceride synthesis in the liver, resulting ultimately in the ectopic lipid deposition and hepatosteatosis. However, apart from liver, dietary fructose may also contribute to the development of metabolic syndrome through deregulation of metabolic pathways in the hypothalamus-adipose tissue axis. In this chapter we summarize the findings on the rat animal model fed with different concentrations of fructose (10% and 60% solutions). The results showed that lower concentration of liquid fructose aggravates hepatic lipid metabolism, while higher fructose load leads to dyslipidemia, visceral adiposity, and leptin resistance, which could be a critical component of the obesity-promoting vicious cycle that results in extreme forms of untreatable obesity.
PB  - Woodhead Publishing
T2  - Production and Management of Beverages
T2  - Production and Management of Beverages
T1  - Managing Metabolic Health Impact of Fructose-Containing Beverages
DO  - 10.1016/B978-0-12-815260-7.00001-8
SP  - 1
EP  - 45
ER  - 

@inbook{
editor = "Grumezescu, Alexandru Mihai, Holban, Alina Maria",
author = "Đorđević, Ana and Veličković, Nataša",
year = "2019",
abstract = "Fructose has been a part of human diet for centuries, but in the last 50 years the consumption of fructose-sweetened soft drinks has risen significantly and it was associated with prevalence of obesity and metabolic syndrome. Fructose overconsumption leads to enhanced de novo lipogenesis and triglyceride synthesis in the liver, resulting ultimately in the ectopic lipid deposition and hepatosteatosis. However, apart from liver, dietary fructose may also contribute to the development of metabolic syndrome through deregulation of metabolic pathways in the hypothalamus-adipose tissue axis. In this chapter we summarize the findings on the rat animal model fed with different concentrations of fructose (10% and 60% solutions). The results showed that lower concentration of liquid fructose aggravates hepatic lipid metabolism, while higher fructose load leads to dyslipidemia, visceral adiposity, and leptin resistance, which could be a critical component of the obesity-promoting vicious cycle that results in extreme forms of untreatable obesity.",
publisher = "Woodhead Publishing",
journal = "Production and Management of Beverages, Production and Management of Beverages",
booktitle = "Managing Metabolic Health Impact of Fructose-Containing Beverages",
doi = "10.1016/B978-0-12-815260-7.00001-8",
pages = "1-45"
}

Grumezescu, A. M., Holban, A. M., Đorđević, A.,& Veličković, N.. (2019). Managing Metabolic Health Impact of Fructose-Containing Beverages. in Production and Management of Beverages
Woodhead Publishing., 1-45.
https://doi.org/10.1016/B978-0-12-815260-7.00001-8

Grumezescu AM, Holban AM, Đorđević A, Veličković N. Managing Metabolic Health Impact of Fructose-Containing Beverages. in Production and Management of Beverages. 2019;:1-45.
doi:10.1016/B978-0-12-815260-7.00001-8 .

Grumezescu, Alexandru Mihai, Holban, Alina Maria, Đorđević, Ana, Veličković, Nataša, "Managing Metabolic Health Impact of Fructose-Containing Beverages" in Production and Management of Beverages (2019):1-45,
https://doi.org/10.1016/B978-0-12-815260-7.00001-8 . .

TY  - JOUR
AU  - Brkljačić, Jelena
AU  - Veličković, Nataša
AU  - Elaković, Ivana
AU  - Teofilović, Ana
AU  - Vojnović-Milutinović, Danijela
AU  - Đorđević, Ana
AU  - Matić, Gordana
PY  - 2019
UR  - http://www.doiserbia.nb.rs/Article.aspx?ID=0354-46641900023N
UR  - http://www.serbiosoc.org.rs/arch/index.php/abs/article/view/4079
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3573
AB  - An increase in fructose consumption coincides with a rising incidence of metabolic disorders. Dietary fructose has been shown to affect hepatic lipid metabolism in a way that may lead to lipid deposition in the liver. In this study, we tested the hypothesis that the effects of fructose overconsumption on hepatic lipid metabolism differ between sexes. To that end we examined the effects of a high-fructose diet on the expression of key enzymes and transcription factors involved in the regulation of fatty acid oxidation and de novo lipogenesis in the liver of 12-week-old male and female Wistar rats. Immediately after weaning, the rats were subjected to a standard diet and 10% fructose solution or drinking water for 9 weeks. The fructose-enriched diet induced hypertriglyceridemia and increased hepatic de novo lipogenesis in both sexes, without lipid deposition in the liver. At the same time, visceral adiposity was observed only in female rats, while in males the treatment stimulated hepatic fatty acid oxidation. The fructose-enriched diet induced sex-specific effects on hepatic lipid metabolism in young rats. These results imply that male and female rats employ different strategies to cope with dietary fructose-related energy overload and to avoid lipid accumulation in the liver.
T2  - Archives of Biological Sciences
T1  - Fructose-enriched diet affects hepatic lipid metabolism in young male and female rats in different ways
IS  - 3
VL  - 71
DO  - 10.2298/ABS190306023N
SP  - 417
EP  - 424
ER  - 

@article{
author = "Brkljačić, Jelena and Veličković, Nataša and Elaković, Ivana and Teofilović, Ana and Vojnović-Milutinović, Danijela and Đorđević, Ana and Matić, Gordana",
year = "2019",
abstract = "An increase in fructose consumption coincides with a rising incidence of metabolic disorders. Dietary fructose has been shown to affect hepatic lipid metabolism in a way that may lead to lipid deposition in the liver. In this study, we tested the hypothesis that the effects of fructose overconsumption on hepatic lipid metabolism differ between sexes. To that end we examined the effects of a high-fructose diet on the expression of key enzymes and transcription factors involved in the regulation of fatty acid oxidation and de novo lipogenesis in the liver of 12-week-old male and female Wistar rats. Immediately after weaning, the rats were subjected to a standard diet and 10% fructose solution or drinking water for 9 weeks. The fructose-enriched diet induced hypertriglyceridemia and increased hepatic de novo lipogenesis in both sexes, without lipid deposition in the liver. At the same time, visceral adiposity was observed only in female rats, while in males the treatment stimulated hepatic fatty acid oxidation. The fructose-enriched diet induced sex-specific effects on hepatic lipid metabolism in young rats. These results imply that male and female rats employ different strategies to cope with dietary fructose-related energy overload and to avoid lipid accumulation in the liver.",
journal = "Archives of Biological Sciences",
title = "Fructose-enriched diet affects hepatic lipid metabolism in young male and female rats in different ways",
number = "3",
volume = "71",
doi = "10.2298/ABS190306023N",
pages = "417-424"
}

Brkljačić, J., Veličković, N., Elaković, I., Teofilović, A., Vojnović-Milutinović, D., Đorđević, A.,& Matić, G.. (2019). Fructose-enriched diet affects hepatic lipid metabolism in young male and female rats in different ways. in Archives of Biological Sciences, 71(3), 417-424.
https://doi.org/10.2298/ABS190306023N

Brkljačić J, Veličković N, Elaković I, Teofilović A, Vojnović-Milutinović D, Đorđević A, Matić G. Fructose-enriched diet affects hepatic lipid metabolism in young male and female rats in different ways. in Archives of Biological Sciences. 2019;71(3):417-424.
doi:10.2298/ABS190306023N .

Brkljačić, Jelena, Veličković, Nataša, Elaković, Ivana, Teofilović, Ana, Vojnović-Milutinović, Danijela, Đorđević, Ana, Matić, Gordana, "Fructose-enriched diet affects hepatic lipid metabolism in young male and female rats in different ways" in Archives of Biological Sciences, 71, no. 3 (2019):417-424,
https://doi.org/10.2298/ABS190306023N . .

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  - 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 . .