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dc.contributor.authorH.I. Majane, Olebogengen_US
dc.contributor.authorVengethasamy, Leandaen_US
dc.contributor.authorF. du Toit, Eugeneen_US
dc.contributor.authorMakaula, Siyandaen_US
dc.contributor.authorJ. Woodiwiss, Angelaen_US
dc.contributor.authorR. Norton, Gavinen_US
dc.date.accessioned2017-04-24T13:06:08Z
dc.date.available2017-04-24T13:06:08Z
dc.date.issued2009en_US
dc.date.modified2010-10-04T06:52:35Z
dc.identifier.issn0194911Xen_US
dc.identifier.doi10.1161/HYPERTENSIONAHA.108.127514en_AU
dc.identifier.urihttp://hdl.handle.net/10072/34341
dc.description.abstractWe explored whether dietary-induced obesity hastens the transition from concentric left ventricular (LV) hypertrophy to pump dysfunction in spontaneously hypertensive rats (SHRs) and the mechanisms thereof. After feeding rats a diet for 4 to 5 months, obesity was induced in SHRs and Wistar-Kyoto (WKY) control rats. Obesity was not associated with abnormal blood glucose control (glycosylated hemoglobin) or with increases in systolic blood pressure. However, in SHRs, but not in WKY rats, obesity was associated with a reduced LV chamber systolic function, as determined by echocardiography, and in isolated perfused heart studies. A marked increase in LV end diastolic diameter and a right shift in the LV diastolic pressure-volume relation were noted in obese SHRs but not in obese WKY rats. Moreover, LV intrinsic myocardial systolic function, as determined from the slope of the linearized LV systolic stress-strain relationship (LV myocardial end systolic elastance), was markedly reduced in obese as compared with lean SHRs, whereas LV myocardial end systolic elastance was maintained in obese WKY rats. Obesity increased LV weight, cardiomyocyte width, cardiomyocyte apoptosis (TUNEL), the activity of myocardial matrix metalloproteinases (zymography), and serum leptin concentrations in SHRs but not in WKY rats. In conclusion, SHRs are susceptible to the adverse effects of dietary-induced obesity on the heart, an effect that hastens the progression from concentric LV hypertrophy to pump dysfunction independent of blood pressure changes or alterations in glycosylated hemoglobin. This effect may be mediated through a proclivity of SHRs to developing both obesity-induced effects on cardiomyocyte apoptosis and activation of myocardial collagenases through leptin resistance and obesity-induced hypertrophy.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_AU
dc.format.extent230262 bytes
dc.format.mimetypeapplication/pdf
dc.languageEnglishen_US
dc.language.isoen_AU
dc.publisherLippincott Williams & Wilkinsen_US
dc.publisher.placeUnited Statesen_US
dc.relation.ispartofstudentpublicationNen_AU
dc.relation.ispartofpagefrom1376en_US
dc.relation.ispartofpageto1383en_US
dc.relation.ispartofissue6en_US
dc.relation.ispartofjournalHypertensionen_US
dc.relation.ispartofvolume54en_US
dc.rights.retentionYen_AU
dc.subject.fieldofresearchPhysiology not elsewhere classifieden_US
dc.subject.fieldofresearchcode060699en_US
dc.titleDietary-Induced Obesity Hastens the Progression From Concentric Cardiac Hypertrophy to Pump Dysfunction in Spontaneously Hypertensive Ratsen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.rights.copyrightCopyright 2009 LWW. This is a non-final version of an article published in final form in Hypertension Volume 54, Issue 6, 1376-1383. Reproduced in accordance with the copyright policy of the publisher. Please refer to the journal link for access to the definitive, published version.en_AU
gro.date.issued2009
gro.hasfulltextFull Text


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