Dietary-Induced Obesity Hastens the Progression From Concentric Cardiac Hypertrophy to Pump Dysfunction in Spontaneously Hypertensive Rats

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Title Dietary-Induced Obesity Hastens the Progression From Concentric Cardiac Hypertrophy to Pump Dysfunction in Spontaneously Hypertensive Rats
Author Majane, Olebogeng H.I.; Vengethasamy, Leanda; Du Toit, Eugene; Makaula, Siyanda; Woodiwiss, Angela J.; Norton, Gavin R.
Journal Name Hypertension
Year Published 2009
Place of publication United States
Publisher Lippincott Williams & Wilkins
Abstract We 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.
Peer Reviewed Yes
Published Yes
Alternative URI http://dx.doi.org/10.1161/HYPERTENSIONAHA.108.127514
Copyright Statement Copyright 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.
Volume 54
Issue Number 6
Page from 1376
Page to 1383
ISSN 0194-911X
Date Accessioned 2010-06-23
Date Available 2010-10-04T06:52:35Z
Language en_AU
Research Centre Griffith Health Institute; Heart Foundation Research Centre
Faculty Griffith Health Faculty
Subject Physiology
URI http://hdl.handle.net/10072/34341
Publication Type Journal Articles (Refereed Article)
Publication Type Code c1x

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