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dc.contributor.authorNduhirabandi, Fredericen_US
dc.contributor.authorDu Toit, Eugeneen_US
dc.contributor.authorBlackhurst, Deeen_US
dc.contributor.authorMarais, Daviden_US
dc.contributor.authorLochner, Amandaen_US
dc.date.accessioned2017-05-03T15:31:44Z
dc.date.available2017-05-03T15:31:44Z
dc.date.issued2011en_US
dc.date.modified2013-05-29T08:08:52Z
dc.identifier.issn07423098en_US
dc.identifier.doi10.1111/j.1600-079X.2010.00826.xen_US
dc.identifier.urihttp://hdl.handle.net/10072/38470
dc.description.abstractObesity, a major risk factor for ischemic heart disease, is associated with increased oxidative stress and reduced antioxidant status. Melatonin, a potent free radical scavenger and antioxidant, has powerful cardioprotective effects in lean animals but its efficacy in obesity is unknown. We investigated the effects of chronic melatonin administration on the development of the metabolic syndrome as well as ischemia-reperfusion injury in a rat model of diet-induced obesity (DIO). Male Wistar rats received a control diet, a control diet with melatonin, a high-calorie diet, or a high-calorie diet with melatonin (DM). Melatonin (4 mg/kg/day) was administered in the drinking water. After 16 wk, biometric and blood metabolic parameters were measured. Hearts were perfused ex vivo for the evaluation of myocardial function, infarct size (IFS) and biochemical changes [activation of PKB/Akt, ERK, p38 MAPK, AMPK, and glucose transporter (GLUT)-4 expression). The high-calorie diet caused increases in body weight (BW), visceral adiposity, serum insulin and triglycerides (TRIG), with no change in glucose levels. Melatonin treatment reduced the BW gain, visceral adiposity, blood TRIG, serum insulin, homeostatic model assessment index and thiobarbituric acid reactive substances in the DIO group. Melatonin reduced IFS in DIO and control groups and increased percentage recovery of functional performance of DIO hearts. During reperfusion, hearts from melatonin-treated rats had increased activation of PKB/Akt, ERK42/44 and reduced p38 MAPK activation. Chronic melatonin treatment prevented the metabolic abnormalities induced by DIO and protected the heart against ischemia-reperfusion injury. These beneficial effects were associated with activation of the reperfusion injury salvage kinases pathway.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_US
dc.languageEnglishen_US
dc.language.isoen_US
dc.publisherWiley-Blackwell Publishing, Inc.en_US
dc.publisher.placeUnited Statesen_US
dc.relation.ispartofstudentpublicationNen_US
dc.relation.ispartofpagefrom171en_US
dc.relation.ispartofpageto182en_US
dc.relation.ispartofissue2en_US
dc.relation.ispartofjournalJournal of Pineal Researchen_US
dc.relation.ispartofvolume50en_US
dc.rights.retentionYen_US
dc.subject.fieldofresearchPhysiology not elsewhere classifieden_US
dc.subject.fieldofresearchcode060699en_US
dc.titleChronic melatonin consumption prevents obesity-related metabolic abnormalities and protects the heart against myocardial ischemia and reperfusion injury in a prediabetic model of diet-induced obesityen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.date.issued2011
gro.hasfulltextNo Full Text


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