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

脂肪酸供应过剩时的营养-内分泌相互作用和肌肉线粒体健康

• 批准号: 355763-2009
• 负责人: Hittel, Dustin
• 金额: $ 1.46万
• 依托单位: University of Calgary
• 依托单位国家: 加拿大
• 项目类别: Discovery Grants Program - Individual
• 财政年份: 2010
• 资助国家: 加拿大
• 起止时间: 2010-01-01 至 2011-12-31
• 项目状态: 已结题
• 来源: https://www.nserc-crsng.gc.ca/ase-oro/Details-Detailles_eng.asp?id=459551
• 关键词: Nutrient; endocrine; interactions; muscle; mitochondrial

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

肥胖大大增加了患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，这是可预防死亡的主要原因之一。这项研究建议的主要假设是，糖尿病前期个体的肌肉过度产生肌生长抑制素，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，细胞动力。这两个发现都很重要，因为随着肥胖发展为2型糖尿病，肌肉功能普遍下降。本研究提案中描述的实验将有助于确定