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

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

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

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

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

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

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

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

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

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

TY  - JOUR
AU  - 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 . .