| Dietary-induced obesity hastens the progression from concentric cardiac hypertrophy to pump dysfunction in spontaneously hypertensive rats. | |
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MedLine Citation:
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PMID: 19841294 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Olebogeng H I Majane; Leanda Vengethasamy; Eugene F du Toit; Siyanda Makaula; Angela J Woodiwiss; Gavin R Norton |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-10-19 |
Journal Detail:
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Title: Hypertension Volume: 54 ISSN: 1524-4563 ISO Abbreviation: Hypertension Publication Date: 2009 Dec |
Date Detail:
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Created Date: 2009-11-20 Completed Date: 2009-12-17 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: United States |
Other Details:
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Languages: eng Pagination: 1376-83 Citation Subset: IM |
Affiliation:
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Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, University of the Witwatersrand Medical School, 7 York Rd, Parktown, 2193 Johannesburg, South Africa. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis Body Weight Cardiomegaly / epidemiology, pathology*, ultrasonography Diastole Disease Models, Animal Disease Progression Eating Echocardiography Hypertension / epidemiology, physiopathology* In Situ Nick-End Labeling Myocytes, Cardiac / pathology* Necrosis Obesity / epidemiology, physiopathology* Organ Size Rats Rats, Inbred SHR Rats, Inbred WKY Risk Factors Systole Ventricular Dysfunction, Left / epidemiology, pathology*, ultrasonography |
| Comments/Corrections | |
Comment In:
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Hypertension. 2009 Dec;54(6):1209-10
[PMID:
19841293
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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