Key result
High caloric diet in rats worsens contractile function and increases infarct size via pre-diabetes.
Why the study?
Obesity and pre-diabetes are associated with cardiovascular diseases, but the impact on mitochondrial respiratory capacity and contractile function in the pre-diabetic heart is unclear.
In a rat model of pre-diabetes, a high caloric diet decreases mitochondrial bioenergetic capacity, which impairs basal contractile function and reduces tolerance to acute oxygen deprivation.
Answers are grounded in this paper and cite their sources.
Pre-diabetic mitochondrial impairment may underlie early cardiac dysfunction; leaves open relevance to human ischemia tolerance and cardiomyopathy.
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.
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Essop et al. (2009) studied Pre-diabetes. High caloric diet vs. Age-matched lean controls was evaluated on Cardiac function and mitochondrial respiratory capacity. A high caloric diet in rats induced pre-diabetes, leading to attenuated baseline contractile function, increased myocardial infarct sizes, and diminished ADP phosphorylation rates compared to controls.
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