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dc.creatorStanišić, Jelena
dc.creatorKorićanac, Goran
dc.creatorĆulafić, Tijana
dc.creatorRomić, Snježana Đ.
dc.creatorStojiljković, Mojca D.
dc.creatorKostić, Milan
dc.creatorPantelić, Marija
dc.creatorTepavčević, Snežana
dc.date.accessioned2018-03-01T16:39:49Z
dc.date.available2018-03-01T16:39:49Z
dc.date.issued2016
dc.identifier.issn0303-7207
dc.identifier.urihttps://vinar.vin.bg.ac.rs/handle/123456789/913
dc.description.abstractIncrease in fructose consumption together with decrease in physical activity contributes to the development of metabolic syndrome and consequently cardiovascular diseases. The current study examined the preventive role of exercise on defects in cardiac insulin signaling and function of endothelial nitric oxide synthase (eNOS) in fructose fed rats. Male Wistar rats were divided into control, sedentary fructose (received 10% fructose for 9 weeks) and exercise fructose (additionally exposed to low intensity exercise) groups. Concentration of triglycerides, glucose, insulin and visceral adipose tissue weight were determined to estimate metabolic syndrome development. Expression and/or phosphorylation of cardiac insulin receptor (IR), insulin receptor substrate 1 (IRS1), tyrosine-specific protein phosphatase 1B (PTP1B), Akt, extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) and eNOS were evaluated. Fructose overload increased visceral adipose tissue, insulin concentration and homeostasis model assessment index. Exercise managed to decrease visceral adiposity and insulin level and to increase insulin sensitivity. Fructose diet increased level of cardiac PTP1B and pIRS1 (Ser307), while levels of IR and ERK1/2, as well as pIRS1 (Tyr 632), pAkt (Ser473, Thr308) and pERK1/2 were decreased. These disturbances were accompanied by reduced phosphorylation of eNOS at Ser1177. Exercise managed to prevent most of the disturbances in insulin signaling caused by fructose diet (except phosphorylation of IRS1 at Tyr 632 and phosphorylation and protein expression of ERK1/2) and consequently restored function of eNOS. Low intensity exercise could be considered as efficient treatment of cardiac insulin resistance induced by fructose diet. (C) 2015 Elsevier Ireland Ltd. All rights reserved.en
dc.publisherElsevier
dc.relationinfo:eu-repo/grantAgreement/MESTD/Integrated and Interdisciplinary Research (IIR or III)/41009/RS//
dc.rightsrestrictedAccessen
dc.sourceMolecular and Cellular Endocrinologyen
dc.subjectLow intensity exerciseen
dc.subjectFructoseen
dc.subjectHearten
dc.subjectInsulin signaling pathwayen
dc.subjectInsulin resistanceen
dc.subjectEndothelial nitric oxide synthaseen
dc.titleLow intensity exercise prevents disturbances in rat cardiac insulin signaling and endothelial nitric oxide synthase induced by high fructose dieten
dc.typearticleen
dc.rights.licenseARR
dcterms.abstractСтанишић Јелена; Корићанац Горан; Ћулафић Тијана; Ромић Сњежана; Стојиљковић Мојца; Костић Милан; Пантелић Марија; Тепавчевић Снежана;
dc.citation.volume420
dc.citation.issueC
dc.citation.spage97
dc.citation.epage104
dc.identifier.wos000368949700010
dc.identifier.doi10.1016/j.mce.2015.11.032
dc.citation.rankM21
dc.identifier.pmid26644274
dc.type.versionpublishedVersion
dc.identifier.scopus2-s2.0-84949557272


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