Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/1592
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dc.contributor.authorVeličković, Natašaen_US
dc.contributor.authorTeofilović, Anaen_US
dc.contributor.authorIlić, Draganaen_US
dc.contributor.authorDjordjevic, Anaen_US
dc.contributor.authorVojnović Milutinović, Danijelaen_US
dc.contributor.authorPetrović, Snježanaen_US
dc.contributor.authorPreitner, Fredericen_US
dc.contributor.authorTappy, Lucen_US
dc.contributor.authorMatić, Gordanaen_US
dc.date.accessioned2019-10-09T07:22:14Z-
dc.date.available2019-10-09T07:22:14Z-
dc.date.issued2019-08-01-
dc.identifier.issn1436-6207-
dc.identifier.urihttps://biore.bio.bg.ac.rs/handle/123456789/1592-
dc.description.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.en_US
dc.language.isoenen_US
dc.relation.ispartofEuropean Journal of Nutritionen_US
dc.subjectAMP-activated protein kinaseen_US
dc.subjectDietary fructoseen_US
dc.subjectInflammationen_US
dc.subjectRat liveren_US
dc.subjectStressen_US
dc.titleModulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stressen_US
dc.typeArticleen_US
dc.identifier.doi10.1007/s00394-018-1730-1-
dc.identifier.pmid29845385-
dc.identifier.scopus2-s2.0-85047661903-
dc.identifier.urlhttps://api.elsevier.com/content/abstract/scopus_id/85047661903-
dc.description.rankM21-
dc.description.impact4.664-
item.languageiso639-1en-
item.cerifentitytypePublications-
item.openairetypeArticle-
item.fulltextWith Fulltext-
item.grantfulltextrestricted-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
crisitem.author.deptChair of Biochemistry and Molecular Biology-
crisitem.author.orcid0000-0002-0142-1056-
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