Dietary Fat Mitochondria and Insulin Signaling

膳食脂肪线粒体和胰岛素信号传导

• 批准号: 7295922
• 负责人: Chad R. Hancock
• 金额: $ 4.53万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-09-01 至 2008-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7295922
• 关键词: Address; Asses; Central obesity; Chad; Citrate; Citrate (si)-Synthase; Citrates; Consumption; Diet; Dietary Fats; Fatty Acids; Fatty acid glycerol esters; Fellowship; Glucose; Goals; Individual; Insulin; Insulin Resistance; Mediating; Mitochondria; Muscle; Muscle Mitochondria; Names; Non-Insulin-Dependent Diabetes Mellitus; Pathogenesis; Phosphorylation; Play; Proto-Oncogene Proteins c-akt; Pyruvate; Pyruvates; Rattus; Regulation; Research; Respiratory Muscles; Role; Skeletal Muscle; Work; base; fatty acid oxidation; feeding; glucose uptake; insulin signaling; oxidation; resistance mechanism; response

DESCRIPTION (provided by applicant): Skeletal muscle plays an integral role in the regulation of the circulating glucose concentration. Thus, the mechanism for skeletal muscle insulin resistance is of great importance for the understanding of the pathogenesis of type-2 diabetes. While a great deal of research has been done on determining what causes skeletal muscle insulin resistance, the mechanism remains unclear. Recent work has suggested that reduced mitochondrial content and/or function in skeletal muscle contributes to insulin resistance and may in fact be genetically determined. It is our hypothesis that the reduction in muscle mitochondria is due to physical inactivity and plays no role in modulating muscle insulin resistance. The primary goal of this study determine the effect of a high fat diet that causes visceral obesity and insulin resistance on skeletal muscle content and functional mitochondria in rats. A second goal is to determine whether insulin stimulated phospohorylation of Akt substrate 160 is impaired in response to high fat feeding.

描述（由申请方提供）：骨骼肌在循环葡萄糖浓度的调节中起着不可或缺的作用。因此，了解骨骼肌胰岛素抵抗的机制对于了解2型糖尿病的发病机制具有重要意义。虽然已经做了大量的研究，以确定是什么原因导致骨骼肌胰岛素抵抗，其机制仍不清楚。最近的研究表明，骨骼肌中线粒体含量和/或功能的减少有助于胰岛素抵抗，实际上可能是由遗传决定的。我们的假设是，肌肉线粒体的减少是由于缺乏体力活动，在调节肌肉胰岛素抵抗方面没有作用。本研究的主要目的是确定导致内脏肥胖和胰岛素抵抗的高脂肪饮食对大鼠骨骼肌含量和功能性线粒体的影响。第二个目标是确定胰岛素刺激的Akt底物160的磷酸化是否响应于高脂肪喂养而受损。