TY  - JOUR
AU  - Shirif, Abdulbaset Zidane
AU  - Kovačević, Sanja
AU  - Brkljačić, Jelena
AU  - Teofilović, Ana
AU  - Elaković, Ivana
AU  - Đorđević, Ana
AU  - Matić, Gordana
PY  - 2021
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4259
AB  - The modern lifestyle brings both excessive fructose consumption and daily exposure
to stress which could lead to metabolic disturbances and type 2 diabetes. Muscles are important
points of glucose and lipid metabolism, with a crucial role in the maintenance of systemic energy
homeostasis. We investigated whether 9-week fructose-enriched diet, with and without exposure to 4-
week unpredictable stress, disturbs insulin signaling in the skeletal muscle of male rats and evaluated
potential contributory roles of muscle lipid metabolism, glucocorticoid signaling and inflammation.
The combination of fructose-enriched diet and stress increased peroxisome proliferator-activated
receptors-  and -  and stimulated lipid uptake, lipolysis and  -oxidation in the muscle of fructosefed
stressed rats. Combination of treatment also decreased systemic insulin sensitivity judged by
lower R-QUICKI, and lowered muscle protein content and stimulatory phosphorylations of insulin
receptor supstrate-1 and Akt, as well as the level of 11 -hydroxysteroid dehydrogenase type 1
and glucocorticoid receptor. At the same time, increased levels of protein tyrosine phosphatase-1B,
nuclear factor- B, tumor necrosis factor- , were observed in the muscle of fructose-fed stressed rats.
Based on these results, we propose that decreased glucocorticoid signaling in the skeletal muscle
can make a setting for lipid-induced inflammation and the development of insulin resistance in
fructose-fed stressed rats.
PB  - Basel, Switzerland: MDPI
T2  - International Journal of Molecular Sciences, Special Issue Glucocorticoids and Metabolic Disorders
T1  - Decreased Glucocorticoid Signaling Potentiates Lipid-Induced Inflammation and Contributes to Insulin Resistance in the Skeletal Muscle of Fructose-Fed Male Rats Exposed to Stress
IS  - 13
VL  - 22
DO  - 10.3390/ijms22137206
SP  - 7206
ER  - 

@article{
author = "Shirif, Abdulbaset Zidane and Kovačević, Sanja and Brkljačić, Jelena and Teofilović, Ana and Elaković, Ivana and Đorđević, Ana and Matić, Gordana",
year = "2021",
abstract = "The modern lifestyle brings both excessive fructose consumption and daily exposure
to stress which could lead to metabolic disturbances and type 2 diabetes. Muscles are important
points of glucose and lipid metabolism, with a crucial role in the maintenance of systemic energy
homeostasis. We investigated whether 9-week fructose-enriched diet, with and without exposure to 4-
week unpredictable stress, disturbs insulin signaling in the skeletal muscle of male rats and evaluated
potential contributory roles of muscle lipid metabolism, glucocorticoid signaling and inflammation.
The combination of fructose-enriched diet and stress increased peroxisome proliferator-activated
receptors-  and -  and stimulated lipid uptake, lipolysis and  -oxidation in the muscle of fructosefed
stressed rats. Combination of treatment also decreased systemic insulin sensitivity judged by
lower R-QUICKI, and lowered muscle protein content and stimulatory phosphorylations of insulin
receptor supstrate-1 and Akt, as well as the level of 11 -hydroxysteroid dehydrogenase type 1
and glucocorticoid receptor. At the same time, increased levels of protein tyrosine phosphatase-1B,
nuclear factor- B, tumor necrosis factor- , were observed in the muscle of fructose-fed stressed rats.
Based on these results, we propose that decreased glucocorticoid signaling in the skeletal muscle
can make a setting for lipid-induced inflammation and the development of insulin resistance in
fructose-fed stressed rats.",
publisher = "Basel, Switzerland: MDPI",
journal = "International Journal of Molecular Sciences, Special Issue Glucocorticoids and Metabolic Disorders",
title = "Decreased Glucocorticoid Signaling Potentiates Lipid-Induced Inflammation and Contributes to Insulin Resistance in the Skeletal Muscle of Fructose-Fed Male Rats Exposed to Stress",
number = "13",
volume = "22",
doi = "10.3390/ijms22137206",
pages = "7206"
}

Shirif, A. Z., Kovačević, S., Brkljačić, J., Teofilović, A., Elaković, I., Đorđević, A.,& Matić, G.. (2021). Decreased Glucocorticoid Signaling Potentiates Lipid-Induced Inflammation and Contributes to Insulin Resistance in the Skeletal Muscle of Fructose-Fed Male Rats Exposed to Stress. in International Journal of Molecular Sciences, Special Issue Glucocorticoids and Metabolic Disorders
Basel, Switzerland: MDPI., 22(13), 7206.
https://doi.org/10.3390/ijms22137206

Shirif AZ, Kovačević S, Brkljačić J, Teofilović A, Elaković I, Đorđević A, Matić G. Decreased Glucocorticoid Signaling Potentiates Lipid-Induced Inflammation and Contributes to Insulin Resistance in the Skeletal Muscle of Fructose-Fed Male Rats Exposed to Stress. in International Journal of Molecular Sciences, Special Issue Glucocorticoids and Metabolic Disorders. 2021;22(13):7206.
doi:10.3390/ijms22137206 .

Shirif, Abdulbaset Zidane, Kovačević, Sanja, Brkljačić, Jelena, Teofilović, Ana, Elaković, Ivana, Đorđević, Ana, Matić, Gordana, "Decreased Glucocorticoid Signaling Potentiates Lipid-Induced Inflammation and Contributes to Insulin Resistance in the Skeletal Muscle of Fructose-Fed Male Rats Exposed to Stress" in International Journal of Molecular Sciences, Special Issue Glucocorticoids and Metabolic Disorders, 22, no. 13 (2021):7206,
https://doi.org/10.3390/ijms22137206 . .

TY  - JOUR
AU  - Kovačević, Sanja
AU  - Elaković, Ivana
AU  - Vojnović-Milutinović, Danijela
AU  - Nikolić-Kokić, Aleksandra
AU  - Blagojević, Duško
AU  - Matić, Gordana
AU  - Tappy, Luc
AU  - Đorđević, Ana
AU  - Brkljačić, Jelena
PY  - 2021
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4468
AB  - Background: Both fructose consumption and chronic stress contribute to the development of metabolic disorders.
The consequences of such combination are not fully understood.
Objective: We investigated whether fructose supplementation and chronic stress synergistically disturb hepatic lipid
and glucose metabolism. The role of energy sensing, redox, and inflammatory status during development of metabolic
disturbances was investigated.
Methods: Female Wistar rats, aged 2.5 mo, were divided into 4 experimental groups: control (C) fed a standard diet
(commercial food and drinking water); fructose (F) fed the same food and 10% fructose solution; stress (S) fed the
standard diet and subjected to chronic unpredictable stress and, stress + fructose (SF) combining conditions F and
S as above. Stress included daily stressors: cold water forced swimming, physical restraint, cold room, wet bedding,
rocking, switching, or tilting cages. After 9 wk, hepatic enzymes and transcription factors involved in gluconeogenesis,
lipogenesis, fatty acid oxidation, antioxidative defence, energy sensing, and cytokines were assessed by qPCR, Western
blotting, and spectrophotometry and analyzed by 2-factor ANOVA.
Results: Fructose increased AMP-activated protein kinase (AMPK) phosphorylation (40%; P < 0.05) and the ratio of
inhibitory phosphorylation to total acetyl-CoA carboxylase (46%; P < 0.01), and decreased sterol regulatory element
binding protein 1c nuclear translocation by 30% (P < 0.05) in F and SF compared with C rats. Increased phosPck
(phoenolpyruvate carboxykinase) (85%) and G6pase (glucose-6-phosphatase) (55%) was observed in S rats (P < 0.05).
A 40% decrease in Apob (apolipoprotein B-100) and an increase in hepatic lipids (P < 0.05), together with a double
increase in TNF-α (P < 0.001), were observed in S rats, but without liver histopathological changes. These stress effects
on lipid accumulation and TNF-α were abolished in SF rats (P < 0.05).
Conclusions: Fructose does not enhance stress effects on hepatic lipid and glucose metabolism but attenuates its
effects on hepatic lipid accumulation and inflammation, suggesting that, in female rats, AMPK activation prevails over
stress-induced effects.
PB  - Oxford University Press on behalf of the American Society of Nutrition
T2  - The Journal of Nutrition
T1  - Fructose-Rich Diet Attenuates Stress-Induced Metabolic Disturbances in the Liver of Adult Female Rats
IS  - 12
VL  - 151
DO  - 10.1093/jn/nxab294
SP  - 3661
EP  - 3670
ER  - 

@article{
author = "Kovačević, Sanja and Elaković, Ivana and Vojnović-Milutinović, Danijela and Nikolić-Kokić, Aleksandra and Blagojević, Duško and Matić, Gordana and Tappy, Luc and Đorđević, Ana and Brkljačić, Jelena",
year = "2021",
abstract = "Background: Both fructose consumption and chronic stress contribute to the development of metabolic disorders.
The consequences of such combination are not fully understood.
Objective: We investigated whether fructose supplementation and chronic stress synergistically disturb hepatic lipid
and glucose metabolism. The role of energy sensing, redox, and inflammatory status during development of metabolic
disturbances was investigated.
Methods: Female Wistar rats, aged 2.5 mo, were divided into 4 experimental groups: control (C) fed a standard diet
(commercial food and drinking water); fructose (F) fed the same food and 10% fructose solution; stress (S) fed the
standard diet and subjected to chronic unpredictable stress and, stress + fructose (SF) combining conditions F and
S as above. Stress included daily stressors: cold water forced swimming, physical restraint, cold room, wet bedding,
rocking, switching, or tilting cages. After 9 wk, hepatic enzymes and transcription factors involved in gluconeogenesis,
lipogenesis, fatty acid oxidation, antioxidative defence, energy sensing, and cytokines were assessed by qPCR, Western
blotting, and spectrophotometry and analyzed by 2-factor ANOVA.
Results: Fructose increased AMP-activated protein kinase (AMPK) phosphorylation (40%; P < 0.05) and the ratio of
inhibitory phosphorylation to total acetyl-CoA carboxylase (46%; P < 0.01), and decreased sterol regulatory element
binding protein 1c nuclear translocation by 30% (P < 0.05) in F and SF compared with C rats. Increased phosPck
(phoenolpyruvate carboxykinase) (85%) and G6pase (glucose-6-phosphatase) (55%) was observed in S rats (P < 0.05).
A 40% decrease in Apob (apolipoprotein B-100) and an increase in hepatic lipids (P < 0.05), together with a double
increase in TNF-α (P < 0.001), were observed in S rats, but without liver histopathological changes. These stress effects
on lipid accumulation and TNF-α were abolished in SF rats (P < 0.05).
Conclusions: Fructose does not enhance stress effects on hepatic lipid and glucose metabolism but attenuates its
effects on hepatic lipid accumulation and inflammation, suggesting that, in female rats, AMPK activation prevails over
stress-induced effects.",
publisher = "Oxford University Press on behalf of the American Society of Nutrition",
journal = "The Journal of Nutrition",
title = "Fructose-Rich Diet Attenuates Stress-Induced Metabolic Disturbances in the Liver of Adult Female Rats",
number = "12",
volume = "151",
doi = "10.1093/jn/nxab294",
pages = "3661-3670"
}

Kovačević, S., Elaković, I., Vojnović-Milutinović, D., Nikolić-Kokić, A., Blagojević, D., Matić, G., Tappy, L., Đorđević, A.,& Brkljačić, J.. (2021). Fructose-Rich Diet Attenuates Stress-Induced Metabolic Disturbances in the Liver of Adult Female Rats. in The Journal of Nutrition
Oxford University Press on behalf of the American Society of Nutrition., 151(12), 3661-3670.
https://doi.org/10.1093/jn/nxab294

Kovačević S, Elaković I, Vojnović-Milutinović D, Nikolić-Kokić A, Blagojević D, Matić G, Tappy L, Đorđević A, Brkljačić J. Fructose-Rich Diet Attenuates Stress-Induced Metabolic Disturbances in the Liver of Adult Female Rats. in The Journal of Nutrition. 2021;151(12):3661-3670.
doi:10.1093/jn/nxab294 .

Kovačević, Sanja, Elaković, Ivana, Vojnović-Milutinović, Danijela, Nikolić-Kokić, Aleksandra, Blagojević, Duško, Matić, Gordana, Tappy, Luc, Đorđević, Ana, Brkljačić, Jelena, "Fructose-Rich Diet Attenuates Stress-Induced Metabolic Disturbances in the Liver of Adult Female Rats" in The Journal of Nutrition, 151, no. 12 (2021):3661-3670,
https://doi.org/10.1093/jn/nxab294 . .

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  - JOUR
AU  - Elaković, Ivana
AU  - Kovačević, Sanja
AU  - Vojnović-Milutinović, Danijela
AU  - Nikolić-Kokić, Aleksandra
AU  - Glban, Alhadi M.
AU  - Spasić, Mihajlo
AU  - Tappy, Luc
AU  - Đorđević, Ana
AU  - Matić, Gordana
AU  - Brkljačić, Jelena
PY  - 2020
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3983
AB  - The effects of early-life fructose consumption on hepatic signaling pathways and their relation to the development of metabolic disorders in later life are not fully understood. To investigate whether fructose over consumption at a young age induces alterations in glucocorticoid signaling that  might  contribute  to  development  of  metabolic  disturbances,  we  analysed  glucocorticoid receptor hormone-binding parameters and expression of its target genes involved in gluconeogenesis (phosphoenolpyruvate carboxykinase and glucose-6-phosphatase) and lipid metabolism (lipin-1),as well as redox and inflammatory status in the liver of female rats subjected to a fructose-rich diet immediately after weaning.  The fructose diet increased hepatic corticosterone concentration,11β-hydroxysteroid  dehydrogenase  type  1  level,   glucocorticoid  receptor  protein  level  and hormone-binding activity, as well as lipin-1 level. The expression of glucose-6-phosphatase was reduced  in  fructose-fed  rats,  while  phosphoenolpyruvate  carboxykinase  remained  unaltered.The  fructose-rich  diet  increased  the  level  of  fructose  transporter  GLUT2,  while  the  expression of  fructolytic  enzymes  fructokinase  and  aldolase  B  remained  unaltered.   The  diet  also  affected pro-inflammatory pathways, but had no effect on the antioxidant defence system.  In conclusion, a fructose-rich diet applied immediately after weaning promoted lipogenesis and enhanced hepatic glucocorticoid signaling, possibly to protect against inflammatory damage, but without an effect on gluconeogenesis and antioxidant enzymes. Yet, prolonged treatment might ultimately lead to more pronounced metabolic disturbances.
PB  - Basel, Switzerland : Multidisciplinary Digital Publishing Institute (MDPI)
T2  - Nutrients
T1  - Fructose Consumption Affects Glucocorticoid Signaling in the Liver of Young Female Rats
IS  - 11
VL  - 12
DO  - 10.3390/nu12113470
SP  - 3470
ER  - 

@article{
author = "Elaković, Ivana and Kovačević, Sanja and Vojnović-Milutinović, Danijela and Nikolić-Kokić, Aleksandra and Glban, Alhadi M. and Spasić, Mihajlo and Tappy, Luc and Đorđević, Ana and Matić, Gordana and Brkljačić, Jelena",
year = "2020",
abstract = "The effects of early-life fructose consumption on hepatic signaling pathways and their relation to the development of metabolic disorders in later life are not fully understood. To investigate whether fructose over consumption at a young age induces alterations in glucocorticoid signaling that  might  contribute  to  development  of  metabolic  disturbances,  we  analysed  glucocorticoid receptor hormone-binding parameters and expression of its target genes involved in gluconeogenesis (phosphoenolpyruvate carboxykinase and glucose-6-phosphatase) and lipid metabolism (lipin-1),as well as redox and inflammatory status in the liver of female rats subjected to a fructose-rich diet immediately after weaning.  The fructose diet increased hepatic corticosterone concentration,11β-hydroxysteroid  dehydrogenase  type  1  level,   glucocorticoid  receptor  protein  level  and hormone-binding activity, as well as lipin-1 level. The expression of glucose-6-phosphatase was reduced  in  fructose-fed  rats,  while  phosphoenolpyruvate  carboxykinase  remained  unaltered.The  fructose-rich  diet  increased  the  level  of  fructose  transporter  GLUT2,  while  the  expression of  fructolytic  enzymes  fructokinase  and  aldolase  B  remained  unaltered.   The  diet  also  affected pro-inflammatory pathways, but had no effect on the antioxidant defence system.  In conclusion, a fructose-rich diet applied immediately after weaning promoted lipogenesis and enhanced hepatic glucocorticoid signaling, possibly to protect against inflammatory damage, but without an effect on gluconeogenesis and antioxidant enzymes. Yet, prolonged treatment might ultimately lead to more pronounced metabolic disturbances.",
publisher = "Basel, Switzerland : Multidisciplinary Digital Publishing Institute (MDPI)",
journal = "Nutrients",
title = "Fructose Consumption Affects Glucocorticoid Signaling in the Liver of Young Female Rats",
number = "11",
volume = "12",
doi = "10.3390/nu12113470",
pages = "3470"
}

Elaković, I., Kovačević, S., Vojnović-Milutinović, D., Nikolić-Kokić, A., Glban, A. M., Spasić, M., Tappy, L., Đorđević, A., Matić, G.,& Brkljačić, J.. (2020). Fructose Consumption Affects Glucocorticoid Signaling in the Liver of Young Female Rats. in Nutrients
Basel, Switzerland : Multidisciplinary Digital Publishing Institute (MDPI)., 12(11), 3470.
https://doi.org/10.3390/nu12113470

Elaković I, Kovačević S, Vojnović-Milutinović D, Nikolić-Kokić A, Glban AM, Spasić M, Tappy L, Đorđević A, Matić G, Brkljačić J. Fructose Consumption Affects Glucocorticoid Signaling in the Liver of Young Female Rats. in Nutrients. 2020;12(11):3470.
doi:10.3390/nu12113470 .

Elaković, Ivana, Kovačević, Sanja, Vojnović-Milutinović, Danijela, Nikolić-Kokić, Aleksandra, Glban, Alhadi M., Spasić, Mihajlo, Tappy, Luc, Đorđević, Ana, Matić, Gordana, Brkljačić, Jelena, "Fructose Consumption Affects Glucocorticoid Signaling in the Liver of Young Female Rats" in Nutrients, 12, no. 11 (2020):3470,
https://doi.org/10.3390/nu12113470 . .

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  - Radovanović, Marina
AU  - Kovačević, Sanja
AU  - Elaković, Ivana
AU  - Vojnović-Milutinović, Danijela
AU  - Matić, Gordana
AU  - Brkljačić, Jelena
PY  - 2019
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5252
AB  - The effects of early-life fructose consumption and their relation to metabolic diseases risk
in adulthood are not yet elucidated. This study explored the direct effects of a diet regime
characterized by fructose enrichment on glucocorticoid receptor signaling in the liver of
female rats immediately after weaning. 21 day-old female Wistar rats were subjected to a 9
week-long diet regime involving standard chow in combination with either the 10%
fructose solution or tap water. Glucocorticoid receptor hormone binding parameters,
intracellular distribution of this molecule as well as the expression of its target genes
involved in lipid metabolism (most notably Lipin-1) and glucose metabolism (PEPCK),
were measured. An increase in the hepatic glucocorticoid receptor hormone binding
activity as well as an elevated nuclear translocation of the receptor, in concert with the
increased protein levels of Lipin-1 were observed after fructose enriched diet. This was
preceeded by a hepatic elevation in Glut-2 fructose transporter expression. Fructose-
enriched diet starting immediately after weaning enhanced hepatic glucocorticoid signaling
in young female rats and promoted lypogenesis as evidenced not only by the lipin-1
increase but also by FAS, ACC and SCREBP-1 expression elevations contributing to
hypertriglyceridemia and the expansion of the visceral adipose tissue 1, with no effect on
the hepatic gluconeogenesis. These results imply that while most parameters remained
within physiological reactivity, prolonged treatment might ultimately lead to more
pronounced metabolic disturbances.
PB  - Belgrade: Faculty of Chemistry
C3  - The 9th Conference of the Serbian Biochemical Society: Diversity in Biochemistry; 2019 Nov 14-16; Belgrade, Serbia
T1  - Fructose consumption affects glucocorticoid receptor signaling and increases lipogenesis in the liver of young female rats
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5252
ER  - 

@conference{
author = "Radovanović, Marina and Kovačević, Sanja and Elaković, Ivana and Vojnović-Milutinović, Danijela and Matić, Gordana and Brkljačić, Jelena",
year = "2019",
abstract = "The effects of early-life fructose consumption and their relation to metabolic diseases risk
in adulthood are not yet elucidated. This study explored the direct effects of a diet regime
characterized by fructose enrichment on glucocorticoid receptor signaling in the liver of
female rats immediately after weaning. 21 day-old female Wistar rats were subjected to a 9
week-long diet regime involving standard chow in combination with either the 10%
fructose solution or tap water. Glucocorticoid receptor hormone binding parameters,
intracellular distribution of this molecule as well as the expression of its target genes
involved in lipid metabolism (most notably Lipin-1) and glucose metabolism (PEPCK),
were measured. An increase in the hepatic glucocorticoid receptor hormone binding
activity as well as an elevated nuclear translocation of the receptor, in concert with the
increased protein levels of Lipin-1 were observed after fructose enriched diet. This was
preceeded by a hepatic elevation in Glut-2 fructose transporter expression. Fructose-
enriched diet starting immediately after weaning enhanced hepatic glucocorticoid signaling
in young female rats and promoted lypogenesis as evidenced not only by the lipin-1
increase but also by FAS, ACC and SCREBP-1 expression elevations contributing to
hypertriglyceridemia and the expansion of the visceral adipose tissue 1, with no effect on
the hepatic gluconeogenesis. These results imply that while most parameters remained
within physiological reactivity, prolonged treatment might ultimately lead to more
pronounced metabolic disturbances.",
publisher = "Belgrade: Faculty of Chemistry",
journal = "The 9th Conference of the Serbian Biochemical Society: Diversity in Biochemistry; 2019 Nov 14-16; Belgrade, Serbia",
title = "Fructose consumption affects glucocorticoid receptor signaling and increases lipogenesis in the liver of young female rats",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5252"
}

Radovanović, M., Kovačević, S., Elaković, I., Vojnović-Milutinović, D., Matić, G.,& Brkljačić, J.. (2019). Fructose consumption affects glucocorticoid receptor signaling and increases lipogenesis in the liver of young female rats. in The 9th Conference of the Serbian Biochemical Society: Diversity in Biochemistry; 2019 Nov 14-16; Belgrade, Serbia
Belgrade: Faculty of Chemistry..
https://hdl.handle.net/21.15107/rcub_ibiss_5252

Radovanović M, Kovačević S, Elaković I, Vojnović-Milutinović D, Matić G, Brkljačić J. Fructose consumption affects glucocorticoid receptor signaling and increases lipogenesis in the liver of young female rats. in The 9th Conference of the Serbian Biochemical Society: Diversity in Biochemistry; 2019 Nov 14-16; Belgrade, Serbia. 2019;.
https://hdl.handle.net/21.15107/rcub_ibiss_5252 .

Radovanović, Marina, Kovačević, Sanja, Elaković, Ivana, Vojnović-Milutinović, Danijela, Matić, Gordana, Brkljačić, Jelena, "Fructose consumption affects glucocorticoid receptor signaling and increases lipogenesis in the liver of young female rats" in The 9th Conference of the Serbian Biochemical Society: Diversity in Biochemistry; 2019 Nov 14-16; Belgrade, Serbia (2019),
https://hdl.handle.net/21.15107/rcub_ibiss_5252 .

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  - CONF
AU  - Kovačević, Sanja
AU  - Đorđević, Ana
AU  - Matić, Gordana
AU  - Elaković, Ivana
PY  - 2019
UR  - https://www.faobmbkl2019.com/abstract-book
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3989
AB  - Modern diet, rich in refined sugars and sweeteners, led to dramatic increase in fructose intake especially in young population. Excessive fructose intake has been associated with growing rate of obesity, insulin resistance and development of metabolic syndrome, women being more prone than men. Chronic low-grade inflammation accompanies obesity and has been implicated in the pathogenesis of obesity-related disorders including metabolic syndrome and insulin resistance. To elucidate whether fructose overconsumption causes inflammation in the visceral adipose tissue (VAT) of young and adult female rats thus contributing to the development of obesity and insulin resistance. We investigated the effects of 9-week fructose-enriched diet applied immediately after weaning (young) or at the 2.5 months of age (adult) on nuclear factor κB (NF-κB) intracellular distribution, and on the expression of pro-inflammatory cytokines (IL-1β, IL-6 and TNFα) in female Wistar rats. Additionally, insulin signalling was analysed at the level of insulin receptor substrate-1 (IRS1), Akt kinase, and their activating and inhibitory phosphorylations. Fructose-enriched diet increased absolute and relative VAT mass in young female rats. There were no changes in VAT mass of adults after fructose diet, even though histological analysis revealed the presence of islets of smaller adipocytes, which indicated adipogenesis. Both young and adult female fructose-fed rats had increased nuclear accumulation of NF-κB and elevated expression of pro-inflammatory cytokines in the VAT. In adults, fructose overconsumption reduced protein content and stimulatory phosphorylation of Akt kinase, while increasing inhibitory phosphorylation of IRS-1. These changes were not observed in young female rats. The results suggest that fructose-enriched diet causes inflammation in VAT of both young and adult female rats. Our work supports the stand that VAT inflammation could represent one of the earliest metabolic perturbations upon fructose overconsumption, since it can occur even before the onset of obesity or insulin resistance. Additionally, only adults developed VAT insulin resistance, indicating age-dependent differences in insulin signalling system and its response to fructose overconsumption in female rats.
PB  - Malaysian Society for Biochemistry and Molecular Biology
PB  - Federation of Asian and Oceanian Biochemists and Molecular Biologists (FAOBMB)
PB  - International Union of Biochemistry and Molecular Biology (IUBMB)
C3  - Kuala Lumpur, Malaysia : 27th FAOBMB & 44th MSBMB Conference Young Scientist Program (YSP)
T1  - Metabolic status of adipose tissue after fructose overconsumption – differences between young and adult female rats
SP  - 3
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_3989
ER  - 

@conference{
author = "Kovačević, Sanja and Đorđević, Ana and Matić, Gordana and Elaković, Ivana",
year = "2019",
abstract = "Modern diet, rich in refined sugars and sweeteners, led to dramatic increase in fructose intake especially in young population. Excessive fructose intake has been associated with growing rate of obesity, insulin resistance and development of metabolic syndrome, women being more prone than men. Chronic low-grade inflammation accompanies obesity and has been implicated in the pathogenesis of obesity-related disorders including metabolic syndrome and insulin resistance. To elucidate whether fructose overconsumption causes inflammation in the visceral adipose tissue (VAT) of young and adult female rats thus contributing to the development of obesity and insulin resistance. We investigated the effects of 9-week fructose-enriched diet applied immediately after weaning (young) or at the 2.5 months of age (adult) on nuclear factor κB (NF-κB) intracellular distribution, and on the expression of pro-inflammatory cytokines (IL-1β, IL-6 and TNFα) in female Wistar rats. Additionally, insulin signalling was analysed at the level of insulin receptor substrate-1 (IRS1), Akt kinase, and their activating and inhibitory phosphorylations. Fructose-enriched diet increased absolute and relative VAT mass in young female rats. There were no changes in VAT mass of adults after fructose diet, even though histological analysis revealed the presence of islets of smaller adipocytes, which indicated adipogenesis. Both young and adult female fructose-fed rats had increased nuclear accumulation of NF-κB and elevated expression of pro-inflammatory cytokines in the VAT. In adults, fructose overconsumption reduced protein content and stimulatory phosphorylation of Akt kinase, while increasing inhibitory phosphorylation of IRS-1. These changes were not observed in young female rats. The results suggest that fructose-enriched diet causes inflammation in VAT of both young and adult female rats. Our work supports the stand that VAT inflammation could represent one of the earliest metabolic perturbations upon fructose overconsumption, since it can occur even before the onset of obesity or insulin resistance. Additionally, only adults developed VAT insulin resistance, indicating age-dependent differences in insulin signalling system and its response to fructose overconsumption in female rats.",
publisher = "Malaysian Society for Biochemistry and Molecular Biology, Federation of Asian and Oceanian Biochemists and Molecular Biologists (FAOBMB), International Union of Biochemistry and Molecular Biology (IUBMB)",
journal = "Kuala Lumpur, Malaysia : 27th FAOBMB & 44th MSBMB Conference Young Scientist Program (YSP)",
title = "Metabolic status of adipose tissue after fructose overconsumption – differences between young and adult female rats",
pages = "3",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_3989"
}

Kovačević, S., Đorđević, A., Matić, G.,& Elaković, I.. (2019). Metabolic status of adipose tissue after fructose overconsumption – differences between young and adult female rats. in Kuala Lumpur, Malaysia : 27th FAOBMB & 44th MSBMB Conference Young Scientist Program (YSP)
Malaysian Society for Biochemistry and Molecular Biology., 3.
https://hdl.handle.net/21.15107/rcub_ibiss_3989

Kovačević S, Đorđević A, Matić G, Elaković I. Metabolic status of adipose tissue after fructose overconsumption – differences between young and adult female rats. in Kuala Lumpur, Malaysia : 27th FAOBMB & 44th MSBMB Conference Young Scientist Program (YSP). 2019;:3.
https://hdl.handle.net/21.15107/rcub_ibiss_3989 .

Kovačević, Sanja, Đorđević, Ana, Matić, Gordana, Elaković, Ivana, "Metabolic status of adipose tissue after fructose overconsumption – differences between young and adult female rats" in Kuala Lumpur, Malaysia : 27th FAOBMB & 44th MSBMB Conference Young Scientist Program (YSP) (2019):3,
https://hdl.handle.net/21.15107/rcub_ibiss_3989 .

TY  - JOUR
AU  - Kovačević, Sanja
AU  - Brkljačić, Jelena
AU  - Matić, Gordana
AU  - Elaković, Ivana
PY  - 2019
UR  - http://www.ncbi.nlm.nih.gov/pubmed/30572328
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3387
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3404
AB  - BACKGROUND Increased fructose consumption and chronic exposure to stress have been associated with the development of obesity and insulin resistance. In the hypothalamus, a crossroad of stress responses and energy balance, insulin and glucocorticoids regulate the expression of orexigenic neuropeptides, neuropeptide Y (NPY) and agouti-related protein (AgRP), and anorexigenic neuropeptides, proopio-melanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART). OBJECTIVES We investigated whether chronic stress and fructose diet disrupt these hormonal signaling pathways and appetite control in the hypothalamus, contributing to the development of insulin resistance and obesity. Potential roles of hypothalamic inflammation and oxidative stress in the development of insulin resistance were also analyzed. METHODS Insulin, glucocorticoid, and leptin signaling, expression of orexigenic and anorexigenic neuropeptides, and antioxidative and inflammatory statuses in the whole hypothalamus of fructose-fed female rats exposed to unpredictable stress for 9 weeks were analyzed using quantitative PCR and Western blotting. RESULTS Chronic stress combined with a fructose-enriched diet reduced protein content and stimulatory phosphorylation of Akt kinase, and elevated 11β-hydroxysteroid dehydrogenase 1 and glucocorticoid receptor expression, while alterations in appetite regulation (NPY, AgRP, POMC, CART, leptin receptor, and SOCS3 expression) were not observed. The expression of antioxidative defense enzymes (mitochondrial manganese superoxide dismutase 2, glutathione reductase, and catalase) and proinflammatory cytokines (IL-1β, IL-6, and TNFα) was reduced. CONCLUSIONS Our results underline the combination of long-term stress exposure and fructose overconsumption as more detrimental for hypothalamic function than for either of the factors separately, as it enhanced glucocorticoid and impaired insulin signaling, antioxidative -defense, and inflammatory responses of this homeostasis- regulating center.
T2  - Neuroendocrinology
T1  - Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats.
DO  - 10.1159/000496391
ER  - 

@article{
author = "Kovačević, Sanja and Brkljačić, Jelena and Matić, Gordana and Elaković, Ivana",
year = "2019",
abstract = "BACKGROUND Increased fructose consumption and chronic exposure to stress have been associated with the development of obesity and insulin resistance. In the hypothalamus, a crossroad of stress responses and energy balance, insulin and glucocorticoids regulate the expression of orexigenic neuropeptides, neuropeptide Y (NPY) and agouti-related protein (AgRP), and anorexigenic neuropeptides, proopio-melanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART). OBJECTIVES We investigated whether chronic stress and fructose diet disrupt these hormonal signaling pathways and appetite control in the hypothalamus, contributing to the development of insulin resistance and obesity. Potential roles of hypothalamic inflammation and oxidative stress in the development of insulin resistance were also analyzed. METHODS Insulin, glucocorticoid, and leptin signaling, expression of orexigenic and anorexigenic neuropeptides, and antioxidative and inflammatory statuses in the whole hypothalamus of fructose-fed female rats exposed to unpredictable stress for 9 weeks were analyzed using quantitative PCR and Western blotting. RESULTS Chronic stress combined with a fructose-enriched diet reduced protein content and stimulatory phosphorylation of Akt kinase, and elevated 11β-hydroxysteroid dehydrogenase 1 and glucocorticoid receptor expression, while alterations in appetite regulation (NPY, AgRP, POMC, CART, leptin receptor, and SOCS3 expression) were not observed. The expression of antioxidative defense enzymes (mitochondrial manganese superoxide dismutase 2, glutathione reductase, and catalase) and proinflammatory cytokines (IL-1β, IL-6, and TNFα) was reduced. CONCLUSIONS Our results underline the combination of long-term stress exposure and fructose overconsumption as more detrimental for hypothalamic function than for either of the factors separately, as it enhanced glucocorticoid and impaired insulin signaling, antioxidative -defense, and inflammatory responses of this homeostasis- regulating center.",
journal = "Neuroendocrinology",
title = "Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats.",
doi = "10.1159/000496391"
}

Kovačević, S., Brkljačić, J., Matić, G.,& Elaković, I.. (2019). Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats.. in Neuroendocrinology.
https://doi.org/10.1159/000496391

Kovačević S, Brkljačić J, Matić G, Elaković I. Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats.. in Neuroendocrinology. 2019;.
doi:10.1159/000496391 .

Kovačević, Sanja, Brkljačić, Jelena, Matić, Gordana, Elaković, Ivana, "Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats." in Neuroendocrinology (2019),
https://doi.org/10.1159/000496391 . .

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

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

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

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

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

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

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

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

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

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

TY  - JOUR
AU  - Kovačević, Sanja
AU  - Brkljačić, Jelena
AU  - Matić, Gordana
AU  - Elaković, Ivana
PY  - 2019
UR  - http://www.ncbi.nlm.nih.gov/pubmed/30572328
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3387
AB  - BACKGROUND Increased fructose consumption and chronic exposure to stress have been associated with the development of obesity and insulin resistance. In the hypothalamus, a crossroad of stress responses and energy balance, insulin and glucocorticoids regulate the expression of orexigenic neuropeptides, neuropeptide Y (NPY) and agouti-related protein (AgRP), and anorexigenic neuropeptides, proopio-melanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART). OBJECTIVES We investigated whether chronic stress and fructose diet disrupt these hormonal signaling pathways and appetite control in the hypothalamus, contributing to the development of insulin resistance and obesity. Potential roles of hypothalamic inflammation and oxidative stress in the development of insulin resistance were also analyzed. METHODS Insulin, glucocorticoid, and leptin signaling, expression of orexigenic and anorexigenic neuropeptides, and antioxidative and inflammatory statuses in the whole hypothalamus of fructose-fed female rats exposed to unpredictable stress for 9 weeks were analyzed using quantitative PCR and Western blotting. RESULTS Chronic stress combined with a fructose-enriched diet reduced protein content and stimulatory phosphorylation of Akt kinase, and elevated 11β-hydroxysteroid dehydrogenase 1 and glucocorticoid receptor expression, while alterations in appetite regulation (NPY, AgRP, POMC, CART, leptin receptor, and SOCS3 expression) were not observed. The expression of antioxidative defense enzymes (mitochondrial manganese superoxide dismutase 2, glutathione reductase, and catalase) and proinflammatory cytokines (IL-1β, IL-6, and TNFα) was reduced. CONCLUSIONS Our results underline the combination of long-term stress exposure and fructose overconsumption as more detrimental for hypothalamic function than for either of the factors separately, as it enhanced glucocorticoid and impaired insulin signaling, antioxidative -defense, and inflammatory responses of this homeostasis- regulating center.
T2  - Neuroendocrinology
T1  - Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats.
IS  - 4
VL  - 108
DO  - 10.1159/000496391
SP  - 278
EP  - 290
ER  - 

@article{
author = "Kovačević, Sanja and Brkljačić, Jelena and Matić, Gordana and Elaković, Ivana",
year = "2019",
abstract = "BACKGROUND Increased fructose consumption and chronic exposure to stress have been associated with the development of obesity and insulin resistance. In the hypothalamus, a crossroad of stress responses and energy balance, insulin and glucocorticoids regulate the expression of orexigenic neuropeptides, neuropeptide Y (NPY) and agouti-related protein (AgRP), and anorexigenic neuropeptides, proopio-melanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART). OBJECTIVES We investigated whether chronic stress and fructose diet disrupt these hormonal signaling pathways and appetite control in the hypothalamus, contributing to the development of insulin resistance and obesity. Potential roles of hypothalamic inflammation and oxidative stress in the development of insulin resistance were also analyzed. METHODS Insulin, glucocorticoid, and leptin signaling, expression of orexigenic and anorexigenic neuropeptides, and antioxidative and inflammatory statuses in the whole hypothalamus of fructose-fed female rats exposed to unpredictable stress for 9 weeks were analyzed using quantitative PCR and Western blotting. RESULTS Chronic stress combined with a fructose-enriched diet reduced protein content and stimulatory phosphorylation of Akt kinase, and elevated 11β-hydroxysteroid dehydrogenase 1 and glucocorticoid receptor expression, while alterations in appetite regulation (NPY, AgRP, POMC, CART, leptin receptor, and SOCS3 expression) were not observed. The expression of antioxidative defense enzymes (mitochondrial manganese superoxide dismutase 2, glutathione reductase, and catalase) and proinflammatory cytokines (IL-1β, IL-6, and TNFα) was reduced. CONCLUSIONS Our results underline the combination of long-term stress exposure and fructose overconsumption as more detrimental for hypothalamic function than for either of the factors separately, as it enhanced glucocorticoid and impaired insulin signaling, antioxidative -defense, and inflammatory responses of this homeostasis- regulating center.",
journal = "Neuroendocrinology",
title = "Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats.",
number = "4",
volume = "108",
doi = "10.1159/000496391",
pages = "278-290"
}

Kovačević, S., Brkljačić, J., Matić, G.,& Elaković, I.. (2019). Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats.. in Neuroendocrinology, 108(4), 278-290.
https://doi.org/10.1159/000496391

Kovačević S, Brkljačić J, Matić G, Elaković I. Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats.. in Neuroendocrinology. 2019;108(4):278-290.
doi:10.1159/000496391 .

Kovačević, Sanja, Brkljačić, Jelena, Matić, Gordana, Elaković, Ivana, "Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats." in Neuroendocrinology, 108, no. 4 (2019):278-290,
https://doi.org/10.1159/000496391 . .

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 . .

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

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

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

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

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

TY  - CONF
AU  - Kovačević, Sanja
AU  - Matić, Gordana
AU  - Elaković, Ivana
PY  - 2018
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3986
AB  - Introduction 
Increased fructose consumption, mainly through sweetened beverages, coincides with growing rate of obesity, women being more prone than men. Chronic low-grade inflammation has been implicated in the pathogenesis of obesity-related disorders including metabolic syndrome and insulin resistance.
The aim 
We investigated whether fructose overconsumption causes inflammation in the visceral adipose tissue (VAT) and hypothalamus of female rats contributing to development of obesity and insulin resistance.
Methods 
Using qPCR and Western blot, we examined the effects of 9-week fructose-enriched diet on inflammatory status, insulin and leptin signaling in the VAT and hypothalamus, as well as on the expression of orexigenic and anorexigenic neuropeptides in the hypothalamus.
Results 
Fructose-fed rats had increased nuclear accumulation of nuclear factor κB (NF-κB) and elevated expression of pro-inflammatory cytokines (IL-1β, IL6, and TNFα), as well as increased protein level of macrophage-specific marker F4/80 in the VAT. In the same tissue, fructose overconsumption reduced protein content and stimulatory phosphorylation of Akt kinase, while increasing inhibitory phosphorylation of insulin receptor substrate-1 (IRS-1). There were no changes in VAT mass, nor in inflammatory markers, insulin and leptin signaling (leptin receptor and SOCS3 expression) and appetite regulation (NPY, AgRP, POMC and CART) in the hypothalamus.
Conclusions 
The results suggest that fructose overconsumption causes alterations in pro-inflammatory markers and reduces insulin signaling in the VAT of female rats. These alterations could be one of the first consequences of fructose overconsumption, since they were detected in the absence of obesity, and hypothalamic inflammation and insulin and leptin resistance.
PB  - Belgrade: Institute for Biological Research “Siniša Stanković”
C3  - Program & Book of Abstracts : IUBMB Advanced School Nutrition, Metabolism and Aging
T1  - Effects Of Fructose-enriched Diet On Inflammation And Insulin Signaling In The Hypothalamus And Visceral Adipose Tissue Of Female Rats
SP  - 34
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_3986
ER  - 

@conference{
editor = "Đorđević, Ana",
author = "Kovačević, Sanja and Matić, Gordana and Elaković, Ivana",
year = "2018",
abstract = "Introduction 
Increased fructose consumption, mainly through sweetened beverages, coincides with growing rate of obesity, women being more prone than men. Chronic low-grade inflammation has been implicated in the pathogenesis of obesity-related disorders including metabolic syndrome and insulin resistance.
The aim 
We investigated whether fructose overconsumption causes inflammation in the visceral adipose tissue (VAT) and hypothalamus of female rats contributing to development of obesity and insulin resistance.
Methods 
Using qPCR and Western blot, we examined the effects of 9-week fructose-enriched diet on inflammatory status, insulin and leptin signaling in the VAT and hypothalamus, as well as on the expression of orexigenic and anorexigenic neuropeptides in the hypothalamus.
Results 
Fructose-fed rats had increased nuclear accumulation of nuclear factor κB (NF-κB) and elevated expression of pro-inflammatory cytokines (IL-1β, IL6, and TNFα), as well as increased protein level of macrophage-specific marker F4/80 in the VAT. In the same tissue, fructose overconsumption reduced protein content and stimulatory phosphorylation of Akt kinase, while increasing inhibitory phosphorylation of insulin receptor substrate-1 (IRS-1). There were no changes in VAT mass, nor in inflammatory markers, insulin and leptin signaling (leptin receptor and SOCS3 expression) and appetite regulation (NPY, AgRP, POMC and CART) in the hypothalamus.
Conclusions 
The results suggest that fructose overconsumption causes alterations in pro-inflammatory markers and reduces insulin signaling in the VAT of female rats. These alterations could be one of the first consequences of fructose overconsumption, since they were detected in the absence of obesity, and hypothalamic inflammation and insulin and leptin resistance.",
publisher = "Belgrade: Institute for Biological Research “Siniša Stanković”",
journal = "Program & Book of Abstracts : IUBMB Advanced School Nutrition, Metabolism and Aging",
title = "Effects Of Fructose-enriched Diet On Inflammation And Insulin Signaling In The Hypothalamus And Visceral Adipose Tissue Of Female Rats",
pages = "34",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_3986"
}

Đorđević, A., Kovačević, S., Matić, G.,& Elaković, I.. (2018). Effects Of Fructose-enriched Diet On Inflammation And Insulin Signaling In The Hypothalamus And Visceral Adipose Tissue Of Female Rats. in Program & Book of Abstracts : IUBMB Advanced School Nutrition, Metabolism and Aging
Belgrade: Institute for Biological Research “Siniša Stanković”., 34.
https://hdl.handle.net/21.15107/rcub_ibiss_3986

Đorđević A, Kovačević S, Matić G, Elaković I. Effects Of Fructose-enriched Diet On Inflammation And Insulin Signaling In The Hypothalamus And Visceral Adipose Tissue Of Female Rats. in Program & Book of Abstracts : IUBMB Advanced School Nutrition, Metabolism and Aging. 2018;:34.
https://hdl.handle.net/21.15107/rcub_ibiss_3986 .

Đorđević, Ana, Kovačević, Sanja, Matić, Gordana, Elaković, Ivana, "Effects Of Fructose-enriched Diet On Inflammation And Insulin Signaling In The Hypothalamus And Visceral Adipose Tissue Of Female Rats" in Program & Book of Abstracts : IUBMB Advanced School Nutrition, Metabolism and Aging (2018):34,
https://hdl.handle.net/21.15107/rcub_ibiss_3986 .

TY  - JOUR
AU  - Savić, Danka
AU  - Knežević, Goran
AU  - Matić, Gordana
AU  - Damjanović, Svetozar
PY  - 2018
UR  - http://www.psyneuen-journal.com/article/S0306-4530(18)30088-X/fulltext
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3034
AB  - BACKGROUND Research results on dehydroepiandrosterone sulfate ester (DHEAS) in post-traumatic stress disorder (PTSD) are inconsistent. We hypothesized that personality traits could be the confounders of DHEAS levels and disease symptoms, which could in part explain the discrepancy in findings. METHOD This study was a part of a broader project in which simultaneous psychological and biological investigations were carried out in hospital conditions. 380 male subjects were categorized in four groups: A) current PTSD (n = 132), B) lifetime PTSD (n = 66), C) trauma controls (n = 101), and D) healthy controls (n = 81), matched by age. RESULTS The level of DHEAS is significantly lower in the current PTSD group than in trauma controls. All groups significantly differ in personality traits Disintegration and Neuroticism (current PTSD group having the highest scores). DHEAS is related to both PTSD and depressive symptoms; however, Structural Equation Model (SEM) shows that the relations are indirect, realized via their confounder - personality trait Disintegration. CONCLUSIONS According to our project results, DHEAS is the second putative biomarker for trauma-related disorders that fails to fulfil this expectation. It appears to be more directly related to personality than to the disease symptoms (the first one being basal cortisol). Our data promote personality as a biologically based construct with seemingly important role in understanding the mental health status.
T2  - Psychoneuroendocrinology
T1  - PTSD and depressive symptoms are linked to DHEAS via personality.
VL  - 92
DO  - 10.1016/j.psyneuen.2018.03.017
SP  - 29
EP  - 33
ER  - 

@article{
author = "Savić, Danka and Knežević, Goran and Matić, Gordana and Damjanović, Svetozar",
year = "2018",
abstract = "BACKGROUND Research results on dehydroepiandrosterone sulfate ester (DHEAS) in post-traumatic stress disorder (PTSD) are inconsistent. We hypothesized that personality traits could be the confounders of DHEAS levels and disease symptoms, which could in part explain the discrepancy in findings. METHOD This study was a part of a broader project in which simultaneous psychological and biological investigations were carried out in hospital conditions. 380 male subjects were categorized in four groups: A) current PTSD (n = 132), B) lifetime PTSD (n = 66), C) trauma controls (n = 101), and D) healthy controls (n = 81), matched by age. RESULTS The level of DHEAS is significantly lower in the current PTSD group than in trauma controls. All groups significantly differ in personality traits Disintegration and Neuroticism (current PTSD group having the highest scores). DHEAS is related to both PTSD and depressive symptoms; however, Structural Equation Model (SEM) shows that the relations are indirect, realized via their confounder - personality trait Disintegration. CONCLUSIONS According to our project results, DHEAS is the second putative biomarker for trauma-related disorders that fails to fulfil this expectation. It appears to be more directly related to personality than to the disease symptoms (the first one being basal cortisol). Our data promote personality as a biologically based construct with seemingly important role in understanding the mental health status.",
journal = "Psychoneuroendocrinology",
title = "PTSD and depressive symptoms are linked to DHEAS via personality.",
volume = "92",
doi = "10.1016/j.psyneuen.2018.03.017",
pages = "29-33"
}

Savić, D., Knežević, G., Matić, G.,& Damjanović, S.. (2018). PTSD and depressive symptoms are linked to DHEAS via personality.. in Psychoneuroendocrinology, 92, 29-33.
https://doi.org/10.1016/j.psyneuen.2018.03.017

Savić D, Knežević G, Matić G, Damjanović S. PTSD and depressive symptoms are linked to DHEAS via personality.. in Psychoneuroendocrinology. 2018;92:29-33.
doi:10.1016/j.psyneuen.2018.03.017 .

Savić, Danka, Knežević, Goran, Matić, Gordana, Damjanović, Svetozar, "PTSD and depressive symptoms are linked to DHEAS via personality." in Psychoneuroendocrinology, 92 (2018):29-33,
https://doi.org/10.1016/j.psyneuen.2018.03.017 . .

TY  - CONF
AU  - Gligorovska, Ljupka
AU  - Teofilović, Ana
AU  - Veličković, Nataša
AU  - Vojnović-Milutinović, Danijela
AU  - Matić, Gordana
AU  - Đorđević, Ana
PY  - 2018
UR  - https://radar.ibiss.bg.ac.rs/handle/handle/123456789/3161
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3321
AB  - Introduction: The macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine involved in the regulation of energy metabolism and glucocorticoid action in the liver. Genetic deletion of Mif may contribute to the development of systemic insulin resistance, especially in the setting of fructose overload that can be associated with perturbed hepatic metabolism. The aim: The aim of the present study was to elucidate the impact of combined effects of Mif deficiency and dietary sugar on energy metabolism 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 energy intake, and indicators of insulin sensitivity and glucocorticoid receptor (GR) signaling. Deregulation of Akt signaling pathway was used as a hallmark of hepatic insulin resistance. Changes in energy metabolism were estimated by AMP-activated protein kinase (AMPK) and SIRT1 protein levels. Results: All fructose-fed animals had increased energy intake, while elevated APMK and SIRT1 protein levels compared to the WT ones. Although enhanced glucocorticoid prereceptor metabolism was observed in all fructose-fed mice, GR protein level was increased only in MIF-/- animals. Mif deficient animals exibited impaired systemic insulin sensitivity. However, the impaired hepatic insulin signaling, revealed by decreased pAkt/total Akt ratio, was observed only in fructose-fed MIF-/- animals. Conclusion: The results showed that Mif deficiency under the conditions of dietary fructose overload leads to systemic insulin resistance, and impaired hepatic insulin signaling and energy metabolism, possibly through enhanced glucocorticoid signaling.
PB  - nstitute for Biological Research "Siniša Stanković"
T1  - Glucocorticoid-mediated effects of mif deficiency and fructose - enriched diet on energy metabolism in the mouse liver
SP  - 17
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_3321
ER  - 

@conference{
author = "Gligorovska, Ljupka and Teofilović, Ana and Veličković, Nataša and Vojnović-Milutinović, Danijela and Matić, Gordana and Đorđević, Ana",
year = "2018",
abstract = "Introduction: The macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine involved in the regulation of energy metabolism and glucocorticoid action in the liver. Genetic deletion of Mif may contribute to the development of systemic insulin resistance, especially in the setting of fructose overload that can be associated with perturbed hepatic metabolism. The aim: The aim of the present study was to elucidate the impact of combined effects of Mif deficiency and dietary sugar on energy metabolism 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 energy intake, and indicators of insulin sensitivity and glucocorticoid receptor (GR) signaling. Deregulation of Akt signaling pathway was used as a hallmark of hepatic insulin resistance. Changes in energy metabolism were estimated by AMP-activated protein kinase (AMPK) and SIRT1 protein levels. Results: All fructose-fed animals had increased energy intake, while elevated APMK and SIRT1 protein levels compared to the WT ones. Although enhanced glucocorticoid prereceptor metabolism was observed in all fructose-fed mice, GR protein level was increased only in MIF-/- animals. Mif deficient animals exibited impaired systemic insulin sensitivity. However, the impaired hepatic insulin signaling, revealed by decreased pAkt/total Akt ratio, was observed only in fructose-fed MIF-/- animals. Conclusion: The results showed that Mif deficiency under the conditions of dietary fructose overload leads to systemic insulin resistance, and impaired hepatic insulin signaling and energy metabolism, possibly through enhanced glucocorticoid signaling.",
publisher = "nstitute for Biological Research "Siniša Stanković"",
title = "Glucocorticoid-mediated effects of mif deficiency and fructose - enriched diet on energy metabolism in the mouse liver",
pages = "17",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_3321"
}

Gligorovska, L., Teofilović, A., Veličković, N., Vojnović-Milutinović, D., Matić, G.,& Đorđević, A.. (2018). Glucocorticoid-mediated effects of mif deficiency and fructose - enriched diet on energy metabolism in the mouse liver. 
nstitute for Biological Research "Siniša Stanković"., 17.
https://hdl.handle.net/21.15107/rcub_ibiss_3321

Gligorovska L, Teofilović A, Veličković N, Vojnović-Milutinović D, Matić G, Đorđević A. Glucocorticoid-mediated effects of mif deficiency and fructose - enriched diet on energy metabolism in the mouse liver. 2018;:17.
https://hdl.handle.net/21.15107/rcub_ibiss_3321 .

Gligorovska, Ljupka, Teofilović, Ana, Veličković, Nataša, Vojnović-Milutinović, Danijela, Matić, Gordana, Đorđević, Ana, "Glucocorticoid-mediated effects of mif deficiency and fructose - enriched diet on energy metabolism in the mouse liver" (2018):17,
https://hdl.handle.net/21.15107/rcub_ibiss_3321 .

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

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

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

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

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

TY  - JOUR
AU  - Veličković, Nataša
AU  - Teofilović, Ana
AU  - Ilić, Dragana
AU  - Đorđević, Ana
AU  - Vojnović-Milutinović, Danijela
AU  - Petrović, Snježana
AU  - Preitner, Frederic
AU  - Tappy, Luc
AU  - Matić, Gordana
PY  - 2018
UR  - http://link.springer.com/10.1007/s00394-018-1730-1
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3077
AB  - PURPOSE High-fructose consumption and chronic stress are both associated with metabolic inflammation and insulin resistance. Recently, disturbed activity of energy sensor AMP-activated protein kinase (AMPK) was recognized as mediator between nutrient-induced stress and inflammation. Thus, we analyzed the effects of high-fructose diet, alone or in combination with chronic stress, on glucose homeostasis, inflammation and expression of energy sensing proteins in the rat liver. METHODS In male Wistar rats exposed to 9-week 20% fructose diet and/or 4-week chronic unpredictable stress we measured plasma and hepatic corticosterone level, indicators of glucose homeostasis and lipid metabolism, hepatic inflammation (pro- and anti-inflammatory cytokine levels, Toll-like receptor 4, NLRP3, activation of NFκB, JNK and ERK pathways) and levels of energy-sensing proteins AMPK, SIRT1 and peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α). RESULTS High-fructose diet led to glucose intolerance, activation of NFκB and JNK pathways and increased intrahepatic IL-1β, TNFα and inhibitory phosphorylation of insulin receptor substrate 1 on Ser307. It also decreased phospho-AMPK/AMPK ratio and increased SIRT1 expression. Stress alone increased plasma and hepatic corticosterone but did not influence glucose tolerance, nor hepatic inflammatory or energy-sensing proteins. After the combined treatment, hepatic corticosterone was increased, glucose tolerance remained preserved, while hepatic inflammation was partially prevented despite decreased AMPK activity. CONCLUSION High-fructose diet resulted in glucose intolerance, hepatic inflammation, decreased AMPK activity and reduced insulin sensitivity. Chronic stress alone did not exert such effects, but when applied together with high-fructose diet it could partially prevent fructose-induced inflammation, presumably due to increased hepatic glucocorticoids.
T2  - European Journal of Nutrition
T1  - Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress.
DO  - 10.1007/s00394-018-1730-1
SP  - 1
EP  - 17
ER  - 

@article{
author = "Veličković, Nataša and Teofilović, Ana and Ilić, Dragana and Đorđević, Ana and Vojnović-Milutinović, Danijela and Petrović, Snježana and Preitner, Frederic and Tappy, Luc and Matić, Gordana",
year = "2018",
abstract = "PURPOSE High-fructose consumption and chronic stress are both associated with metabolic inflammation and insulin resistance. Recently, disturbed activity of energy sensor AMP-activated protein kinase (AMPK) was recognized as mediator between nutrient-induced stress and inflammation. Thus, we analyzed the effects of high-fructose diet, alone or in combination with chronic stress, on glucose homeostasis, inflammation and expression of energy sensing proteins in the rat liver. METHODS In male Wistar rats exposed to 9-week 20% fructose diet and/or 4-week chronic unpredictable stress we measured plasma and hepatic corticosterone level, indicators of glucose homeostasis and lipid metabolism, hepatic inflammation (pro- and anti-inflammatory cytokine levels, Toll-like receptor 4, NLRP3, activation of NFκB, JNK and ERK pathways) and levels of energy-sensing proteins AMPK, SIRT1 and peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α). RESULTS High-fructose diet led to glucose intolerance, activation of NFκB and JNK pathways and increased intrahepatic IL-1β, TNFα and inhibitory phosphorylation of insulin receptor substrate 1 on Ser307. It also decreased phospho-AMPK/AMPK ratio and increased SIRT1 expression. Stress alone increased plasma and hepatic corticosterone but did not influence glucose tolerance, nor hepatic inflammatory or energy-sensing proteins. After the combined treatment, hepatic corticosterone was increased, glucose tolerance remained preserved, while hepatic inflammation was partially prevented despite decreased AMPK activity. CONCLUSION High-fructose diet resulted in glucose intolerance, hepatic inflammation, decreased AMPK activity and reduced insulin sensitivity. Chronic stress alone did not exert such effects, but when applied together with high-fructose diet it could partially prevent fructose-induced inflammation, presumably due to increased hepatic glucocorticoids.",
journal = "European Journal of Nutrition",
title = "Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress.",
doi = "10.1007/s00394-018-1730-1",
pages = "1-17"
}

Veličković, N., Teofilović, A., Ilić, D., Đorđević, A., Vojnović-Milutinović, D., Petrović, S., Preitner, F., Tappy, L.,& Matić, G.. (2018). Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress.. in European Journal of Nutrition, 1-17.
https://doi.org/10.1007/s00394-018-1730-1

Veličković N, Teofilović A, Ilić D, Đorđević A, Vojnović-Milutinović D, Petrović S, Preitner F, Tappy L, Matić G. Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress.. in European Journal of Nutrition. 2018;:1-17.
doi:10.1007/s00394-018-1730-1 .

Veličković, Nataša, Teofilović, Ana, Ilić, Dragana, Đorđević, Ana, Vojnović-Milutinović, Danijela, Petrović, Snježana, Preitner, Frederic, Tappy, Luc, Matić, Gordana, "Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress." in European Journal of Nutrition (2018):1-17,
https://doi.org/10.1007/s00394-018-1730-1 . .

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

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

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

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

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