DISUSE MUSCLE ATROPHY--MECHANISM OF DEVELOPMENT

废用性肌萎缩——发展机制

• 批准号: 6246314
• 负责人: CHARLES A STUART
• 金额: $ 2.71万
• 依托单位: UNIVERSITY OF TEXAS MED BR GALVESTON
• 依托单位国家: 美国
• 财政年份: 1997
• 资助国家: 美国
• 起止时间: 1997-01-06 至 1997-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6246314
• 关键词: atrophy; clinical research; gene expression; human subject; insulinlike growth factor; messenger RNA; muscle metabolism; protein biosynthesis; rest; restricted physical activity; striated muscles

Tests the hypothesis that a direct consequence of muscular inactivity in man is decreased skeletal muscle protein synthesis and that activity related modulation of protein synthesis is mediated via changes in local production of insulin like growth factor I (IGF-I). The protein synthetic rate in skeletal muscle will be directly measured in normal volunteers subjected to absolute bedrest for seven days. Molecular biology techniques will be employed to quantitate alterations in skeletal muscle messenger RNA and IGF-I.

检验以下假设，即肌肉无效的直接结果 人的骨骼肌蛋白质合成减少，该活性 蛋白质合成的相关调节是通过局部变化介导的 产生胰岛素像生长因子I（IGF-I）。 蛋白质 骨骼肌的合成率将直接在正常状态下测量 志愿者遭受了绝对的卧床7天。分子 生物学技术将用于定量改变 骨骼肌使者RNA和IGF-I。