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Cardiac mitochondrial respiration in two rodent models of obesity

Includes bibliographical references (leaves 95-107)

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Bibliographic Details
Main Author: Chan, Wing Yin Anna
Other Authors: Essop, Faadiel
Format: Thesis
Language:English
Published: Department of Medicine 2014
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access_status_str Open Access
author Chan, Wing Yin Anna
author2 Essop, Faadiel
author_browse Chan, Wing Yin Anna
Essop, Faadiel
author_facet Essop, Faadiel
Chan, Wing Yin Anna
author_sort Chan, Wing Yin Anna
collection Thesis
description Includes bibliographical references (leaves 95-107)
format Thesis
id oai:open.uct.ac.za:11427/3371
institution University of Cape Town (South Africa)
language eng
last_indexed 2026-06-10T12:38:54.432Z
license_str Not specified — see source repository
provenance_str_mv Harvested via OAI-PMH from UCTD — University of Cape Town Open Access Repository
publishDate 2014
publishDateRange 2014
publishDateSort 2014
publisher Department of Medicine
publisherStr Department of Medicine
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source_str UCTD — University of Cape Town Open Access Repository
spelling oai:open.uct.ac.za:11427/3371 Cardiac mitochondrial respiration in two rodent models of obesity Chan, Wing Yin Anna Essop, Faadiel Medicine Includes bibliographical references (leaves 95-107) Obesity is a major contributor to the global burden of disease and is closely associated with the development of type II diabetes. Recent studies have demonstrated that increased circulating free fatty acid (FFA) levels may have detrimental effects on the diabetic heart. In this study, we hypothesized that with obesity and obesity-induced insulin resistance/type II diabetes, increased FFA supply decreases cardiac mitochondrial bioenergetic capacity. Furthermore, we also hypothesized that females possess innate cardioprotective programs that will result in enhanced bioenergetic capacity compared to males. We examined our hypothesis employing two rodent models i.e. a) a rat model of diet-induced obesity and b) a transgenic (leptin receptor deficient) mouse model of obesity-induced type II diabetes. For the diabetic mouse model, we determined cardiac mitochondrial respiratory function in an age-dependent (10-12, 18-20 and 55-56 weeks) and gender-dependent (male versus female) manner. We found impaired mitochondrial respiratory capacity in obese rats in baseline and when isolated mitochondria were stressed by anoxia-reoxygenation. We speculate that this may be dure to reduced expression of mitochondrial respiratory chain complexes in the insulin resistant rat heart. For the mouse model and type II diabetes we found increased respiratory capacity at 10-12 weeks, thought to respresent the stage of metabolic syndrome, with no evidence of oxygen wastage or reduction of respiratory capacity. However, 18-20 week-old obese mice were unable to increase respiratory capacity. We also found increased mitochondrial ultrastructural damage and intracellular lipid accumulation in 18-20 week-old diabetic mouse hearts. We propose that this occurs as a result of a mismatch between increased FA uptake and decreased FA oxidative capacity. 2014-07-29T09:02:56Z 2014-07-29T09:02:56Z 2006 Master Thesis Masters MSc http://hdl.handle.net/11427/3371 eng application/pdf Department of Medicine Faculty of Health Sciences University of Cape Town
spellingShingle Medicine
Chan, Wing Yin Anna
Cardiac mitochondrial respiration in two rodent models of obesity
thesis_degree_str Master's
title Cardiac mitochondrial respiration in two rodent models of obesity
title_full Cardiac mitochondrial respiration in two rodent models of obesity
title_fullStr Cardiac mitochondrial respiration in two rodent models of obesity
title_full_unstemmed Cardiac mitochondrial respiration in two rodent models of obesity
title_short Cardiac mitochondrial respiration in two rodent models of obesity
title_sort cardiac mitochondrial respiration in two rodent models of obesity
topic Medicine
url http://hdl.handle.net/11427/3371
work_keys_str_mv AT chanwingyinanna cardiacmitochondrialrespirationintworodentmodelsofobesity