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dc.contributor.authorF. du Toit, Eugeneen_US
dc.contributor.authorSmith, Wayneen_US
dc.contributor.authorMuller, Christoen_US
dc.contributor.authorStrijdom, Hansen_US
dc.contributor.authorStouthammer, Bernadetteen_US
dc.contributor.authorJ. Woodiwiss, Angelaen_US
dc.contributor.authorR. Norton, Gavinen_US
dc.contributor.authorLochner, Amandaen_US
dc.date.accessioned2017-04-24T13:06:15Z
dc.date.available2017-04-24T13:06:15Z
dc.date.issued2008en_US
dc.date.modified2011-10-17T07:26:02Z
dc.identifier.issn03636135en_US
dc.identifier.doi10.1152/ajpheart.00481.2007en_AU
dc.identifier.urihttp://hdl.handle.net/10072/26729
dc.description.abstractWe assessed the myocardial susceptibility to ischemic-reperfusion injury in obese rat hearts in the absence and the presence of predicted circulating concentrations of insulin and fatty acids. Feeding rats a high-calorie diet resulted in increases in body weight, visceral fat content, cardiac hypertrophy, plasma insulin, nonesterified free fatty acid, and triglyceride concentrations. In the absence of both insulin and fatty acids in the coronary perfusate, the hearts of obese rats developed an increased infarct size (41.9 ᠱ.9% for obese vs. 22.9 ᠲ.3% for control, P < 0.05) and a reduced percent recovery of aortic output (4.2 ᠴ.2% for obese vs. 27.7 ᠳ.4% for controls, P < 0.05) after coronary artery occlusion and reperfusion. In the presence of insulin in the coronary perfusate, a cardioprotective effect was noted in both groups, an action that was greater in hearts from obese compared with control rats and which abolished the obesity-induced changes in infarct size (13.8 ᠱ.2% for controls vs. 21.0 ᠱ.6% for obese), and percent recovery of aortic output (60.2 ᠴ.7% for controls vs. 45.7 ᠹ.4% for obese). Fatty acids (0.7 mM, control; and 1.5 mM, obese) added to the coronary perfusate with in vivo concentrations of insulin dramatically increased infarct size (48.2 ᠳ.1% for obese, and 37.5 ᠲ.7% for control; P < 0.05 vs. without fatty acids) and decreased percent aortic output recovery (control, 10.4 ᠵ.2%, and obese 7.8 ᠳ.5%; P < 0.05 vs. without fatty acids) in both groups to similar values. In conclusion, in obesity, the impact of an increased susceptibility of the myocardium to ischemic-reperfusion injury on myocardial injury is likely to be overshadowed by the comparatively greater roles played by predicted increases in circulating insulin and fatty acids found in vivo. These data support the notion that adiposity per se is unlikely to be a valuable predictor of outcomes in ischemic-reperfusion injury.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_AU
dc.languageEnglishen_US
dc.language.isoen_AU
dc.publisherAmerican Physiological Societyen_US
dc.publisher.placeBethesda, USA.en_US
dc.publisher.urihttp://ajpcon.physiology.org/en_AU
dc.relation.ispartofstudentpublicationNen_AU
dc.relation.ispartofpagefromH2336en_US
dc.relation.ispartofpagetoH2343en_US
dc.relation.ispartofjournalAmerican Journal of Physiologyen_US
dc.relation.ispartofvolume294en_US
dc.rights.retentionYen_AU
dc.subject.fieldofresearchCardiology (incl. Cardiovascular Diseases)en_US
dc.subject.fieldofresearchcode110201en_US
dc.titleMyocardial susceptibility to ischemic-reperfusion injury in a prediabetic model of dietary-induced obesityen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.rights.copyrightSelf-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the author[s] for more information.en_AU
gro.date.issued2008
gro.hasfulltextNo Full Text


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