运动诱导的骨骼肌信号机制

背景：运动可通过增强骨骼肌葡萄糖转运及胰岛素活动,来调节葡萄糖内环境。明确这些复杂过程的分子机制将无疑为治疗提供更多的靶向,也为认识这些复杂的生理过程提供最基本的知识。目的：综述运动诱导骨骼肌葡萄糖转运的分子信号机制。方法：以“骨骼肌,运动,腺苷酸活化蛋白激酶,葡萄糖摄取,葡萄糖运载体4”为中文检索词,以“skeletal muscle, exercise, AMPK, glucose uptake, GLUT4”为英文检索词。应用计算机检索PubMed数据库和中文期刊全文数据库2011年11月前发表有关运动诱导骨骼肌信号机制的研究文献,排除重复性研究及Meta分析类文章。共保留39篇文献进行综述。结果与结论：运动/收缩和胰岛素是骨骼肌葡萄糖转运的最有效的和生理相关的刺激,运动诱导的信号机制代表着糖尿病治疗药物学靶点发展的一个重要步骤。运动是通过增加骨骼肌葡萄糖摄取来改善葡萄糖内环境的,而运动诱导的葡萄糖摄取是有多种信号途径来介导的,包括腺苷酸活化蛋白激酶、非典型蛋白激酶C、钙调节依赖蛋白激酶及相对分子质量为160 000的Akt底物等。这些骨骼肌信号机制通过刺激葡萄糖运载体4活动增加来调节葡萄糖的转运。

Exercise-induced signaling mechanisms in skeletal muscle

BACKGROUND:Exercise can regulate glucose homeostasis by enhancing glucose transport and insulin action in contracting skeletal muscle. The definitude of the comprehensive molecular mechanism will undoubtedly provide more targets for treatment, as well as provide fundamental knowledge for this complex physiological process.OBJECTIVE:To review the molecular signals underlying mechanisms exercise-induced glucose transport in skeletal muscle.METHODS:Databases of PubMed and CNKI were searched by computer with the key words of “skeletal muscles, exercise, AMPK, glucose uptake, GLUT4” both in English and Chinese, respectively. Literatures concerning signaling mechanisms of skeletal muscles induced by exercises and published before 2011-11 were collected. Repetitive researches and Meta analysis articles were excluded. Totally 39 articles were included to review.RESULTS AND CONCLUSION:Exercises /contract and insulin are the most effective and physiological stimulation. The signals mechanism induced by exercises has represented an important step of targets development in diabetes treatment drug. Exercises have improved glucose homeostasis by enhancing glucose ingestion in skeletal muscle. And the glucose ingestion induced by exercises is mediated by multiple signal pathways, including adenosine monophosphate-activated protein kinase, atypical protein kinase C, Ca²⁺/calmodulin-dependent protein kinases and AS160. The signals mechanisms in skeletal muscle regulate the glucose transport by stimulating the increase of the exercise of glucose transporter 4.