Nutrient-endocrine interactions and muscle mitochondrial health with fatty acid oversupply

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Obesity dramatically increases the risk for developing type 2 diabetes and cardiovascular disease, the number 1 killer of adults in Canada. According to current estimates over 6.8 million adult Canadians are obese placing it among the leadingcauses of preventable death. The primary hypothesis of this research proposal is that muscle of pre-diabetic individuals overproduces myostatin, a circulating protein that regulates muscle size and function and may contribute to disease progression. Our secondary hypothesis is that high levels of circulating fat damages muscle mitochondria, the cellular powerhouses. These finding are both important because there is a general decline in muscle function with the progression ofobesity to full-blown type 2 diabetes. The experiments described in this research proposal will help determine the role of