Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/1592
Title: Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress
Authors: Veličković, Nataša
Teofilović, Ana
Ilić, Dragana
Djordjevic, Ana
Vojnović Milutinović, Danijela
Petrović, Snježana
Preitner, Frederic
Tappy, Luc
Matić, Gordana 
Keywords: AMP-activated protein kinase;Dietary fructose;Inflammation;Rat liver;Stress
Issue Date: 1-Aug-2019
Rank: M21
Journal: European Journal of Nutrition
Abstract: 
© 2018, Springer-Verlag GmbH Germany, part of Springer Nature. 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.
URI: https://biore.bio.bg.ac.rs/handle/123456789/1592
ISSN: 1436-6207
DOI: 10.1007/s00394-018-1730-1
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