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dc.contributor.authorMaarman, Geralden_US
dc.contributor.authorMarais, Ernaen_US
dc.contributor.authorLochner, Amandaen_US
dc.contributor.authorDu Toit, Eugeneen_US
dc.date.accessioned2017-05-03T15:31:47Z
dc.date.available2017-05-03T15:31:47Z
dc.date.issued2012en_US
dc.date.modified2013-06-03T04:32:50Z
dc.identifier.issn09203206en_US
dc.identifier.doi10.1007/s10557-012-6377-1en_US
dc.identifier.urihttp://hdl.handle.net/10072/47274
dc.description.abstractPurpose By increasing circulating free fatty acids and the rate of fatty acid oxidation, obesity decreases glucose oxidation and myocardial tolerance to ischemia. Partial inhibition of fatty acid oxidation may improve myocardial tolerance to ischemia/reperfusion (I/R) in obesity. We assessed the effects of oxfenicine treatment on post ischemic cardiac function and myocardial infarct size in obese rats. Methods Male Wistar rats were fed a control diet or a high calorie diet which resulted in diet induced obesity (DIO) for 16 weeks. Oxfenicine (200 mg/kg/day) was administered to control and DIO rats for the last 8 weeks. Isolated hearts were perfused and infarct size and post ischemic cardiac function was assessed after regional or global ischemia and reperfusion. Cardiac mitochondrial function was assessed and myocardial expression and activity of CPT-1 (carnitine palmitoyl transferase-1) and IRS-1 (insulin receptor substrate-1) was assessed using Western blot analysis. Results In the DIO rats, chronic oxfenicine treatment improved post ischemic cardiac function and reducedmyocardial infarct size after I/R but had no effect on the cardiac mitochondrial respiration. Chronic oxfenicine treatment worsened post ischemic cardiac function, myocardial infarct size and basal mitochondrial respiration in control rat hearts. Basal respiratory control index (RCI) values, state 2 and state 4 respiration rates and ADP phosphorylation rates were compromised by oxfenicine treatment. Conclusion Chronic oxfenicine treatment improved myocardial tolerance to I/R in the obese rat hearts but decreased myocardial tolerance to I/R in control rat hearts. This decreased tolerance to ischemia of oxfenicine treated controls was associated with adverse changes in basal and reoxygenation mitochondrial function. These changes were absent in oxfenicine treated hearts from obese rats.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_US
dc.languageEnglishen_US
dc.language.isoen_US
dc.publisherSpringeren_US
dc.publisher.placeUnited Statesen_US
dc.relation.ispartofstudentpublicationNen_US
dc.relation.ispartofpagefrom205en_US
dc.relation.ispartofpageto216en_US
dc.relation.ispartofissue3en_US
dc.relation.ispartofjournalCardiovascular Drugs and Therapyen_US
dc.relation.ispartofvolume26en_US
dc.rights.retentionYen_US
dc.subject.fieldofresearchCardiology (incl. Cardiovascular Diseases)en_US
dc.subject.fieldofresearchcode110201en_US
dc.titleEffect of Chronic CPT-1 Inhibition on Myocardial Ischemia-Reperfusion Injury (I/R) in a 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.issued2012
gro.hasfulltextNo Full Text


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