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Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress
dc.creator | Velicković, Nataša | |
dc.creator | Teofilović, Ana | |
dc.creator | Ilić, Dragana | |
dc.creator | Đorđević, Ana | |
dc.creator | Vojnović-Milutinović, Danijela | |
dc.creator | Petrović, Snježana | |
dc.creator | Preitner, Frederic | |
dc.creator | Tappy, Luc | |
dc.creator | Matić, Gordana | |
dc.date.accessioned | 2021-04-20T13:01:03Z | |
dc.date.available | 2021-04-20T13:01:03Z | |
dc.date.issued | 2019 | |
dc.identifier.issn | 1436-6207 | |
dc.identifier.uri | http://rimi.imi.bg.ac.rs/handle/123456789/913 | |
dc.description.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 NF kappa B, JNK and ERK pathways) and levels of energy-sensing proteins AMPK, SIRT1 and peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha). Results High-fructose diet led to glucose intolerance, activation of NF kappa B and JNK pathways and increased intrahepatic IL-1 beta, TNF alpha and inhibitory phosphorylation of insulin receptor substrate 1 on Ser(307). 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. | en |
dc.publisher | Springer Heidelberg, Heidelberg | |
dc.relation | info:eu-repo/grantAgreement/MESTD/Integrated and Interdisciplinary Research (IIR or III)/41009/RS// | |
dc.relation | SCOPES JRP [IZ73ZO_152331] | |
dc.rights | openAccess | |
dc.source | European Journal of Nutrition | |
dc.subject | Inflammation | en |
dc.subject | AMP-activated protein kinase | en |
dc.subject | Dietary fructose | en |
dc.subject | Stress | en |
dc.subject | Rat liver | en |
dc.title | Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress | en |
dc.type | article | |
dc.rights.license | ARR | |
dc.citation.epage | 1845 | |
dc.citation.issue | 5 | |
dc.citation.other | 58(5): 1829-1845 | |
dc.citation.rank | M21 | |
dc.citation.spage | 1829 | |
dc.citation.volume | 58 | |
dc.identifier.doi | 10.1007/s00394-018-1730-1 | |
dc.identifier.fulltext | http://rimi.imi.bg.ac.rs/bitstream/id/713/910.pdf | |
dc.identifier.pmid | 29845385 | |
dc.identifier.scopus | 2-s2.0-85047661903 | |
dc.identifier.wos | 000476492800007 | |
dc.type.version | publishedVersion |