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 . .