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  • Impaired contractile function and mitochondrial respiratory capacity in response to oxygen deprivation in a rat model of pre-diabetes

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    Author(s)
    Essop, MF
    Anna Chan, WY
    Valle, A
    García-Palmer, FJ
    Du Toit, EF
    Griffith University Author(s)
    Du Toit, Eugene
    Year published
    2009
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    Abstract
    Aim: Obesity is a major contributor to the global burden of disease and is closely associated with the development of type 2 diabetes and cardiovascular diseases. This study tested the hypothesis that mitochondrial respiratory capacity of the pre-diabetic heart is decreased leading to impaired contractile function and tolerance to ischaemia/reperfusion. Methods: Eight-week-old male Wistar rats were fed a high caloric diet for 16 weeks after which anthropometric, metabolic, cardiac and mitochondrial parameters were evaluated vs. age-matched lean controls. Cardiac function (working heart perfusions) and mitochondrial ...
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    Aim: Obesity is a major contributor to the global burden of disease and is closely associated with the development of type 2 diabetes and cardiovascular diseases. This study tested the hypothesis that mitochondrial respiratory capacity of the pre-diabetic heart is decreased leading to impaired contractile function and tolerance to ischaemia/reperfusion. Methods: Eight-week-old male Wistar rats were fed a high caloric diet for 16 weeks after which anthropometric, metabolic, cardiac and mitochondrial parameters were evaluated vs. age-matched lean controls. Cardiac function (working heart perfusions) and mitochondrial respiratory capacity were assessed at baseline and in response to acute oxygen deprivation. Results: Rats fed the high caloric diet exhibited increased body weight and visceral fat vs. the control group. Heart weights of obese rats were also increased. Triglyceride, fasting plasma insulin and free fatty acid levels were elevated, while high-density lipoprotein cholesterol levels were reduced in the obese group. Contractile function was attenuated at baseline and further decreased after subjecting hearts to ischaemia-reperfusion. Myocardial infarct sizes were increased while ADP phosphorylation rates were diminished in obese rats. However, no differences were found for mtDNA levels and the degree of oxidative stress-induced damage. Conclusions: These data show that decreased mitochondrial bioenergetic capacity in pre-diabetic rat hearts may impair respiratory capacity and reduce basal contractile function and tolerance to acute oxygen deprivation. Keywords metabolic syndrome, mitochondrial respiration, myocardial infarction, obesity.
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    Journal Title
    Acta Physiologica
    Volume
    197
    Issue
    4
    DOI
    https://doi.org/10.1111/j.1748-1716.2009.02024.x
    Copyright Statement
    Author Posting. Copyright 2009 The Authors. This is the author's version of the work. It is posted here for personal use, not for redistribution. The definitive version was published in Acta Physiologica, Volume 197, Issue 4,289-296, 10.1111/j.1748-1716.2009.02024.x
    Subject
    Zoology not elsewhere classified
    Sports science and exercise
    Medical physiology
    Publication URI
    http://hdl.handle.net/10072/34247
    Collection
    • Journal articles

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