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

肥胖极大地增加了患2型糖尿病和心血管疾病的风险，这是加拿大成年人的头号杀手。根据目前的估计，超过680万加拿大成年人肥胖，使其成为可预防死亡的主要原因之一。本研究建议的主要假设是，糖尿病前期个体的肌肉过量产生肌肉生长抑制素，这是一种调节肌肉大小和功能的循环蛋白，可能有助于疾病的进展。我们的第二个假设是，高水平的循环脂肪会损害肌肉线粒体，而线粒体是细胞的能量来源。这些发现都很重要，因为随着肥胖发展为全面的2型糖尿病，肌肉功能普遍下降。在这个研究计划中描述的实验将有助于确定的作用

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