天津体育学院学报2025，Vol.40Issue(3)：322-330,9.DOI:10.13297/j.cnki.issn1005-0000.2025.03.010
运动改善糖尿病骨骼肌萎缩的研究进展与展望
Research Progress of Exercise Improving Skeletal Muscle Atrophy in Diabetes
摘要
Abstract
The phosphatidylinositol-3-kinase/protein kinase B(PI3K/AKT)pathway plays a core role in metabolic regulation,and insulin resistance leads to impaired activation of the PI3K/AKT pathway,triggering metabolic diseases.Insulin resistance in diabetes inhibits PI3K/AKT signaling pathway and then inhibits skeletal muscle protein synthesis,causing skeletal muscle atrophy.Exercise promotes the translocation of glucose transporter 4(GLUT4)in skeletal muscle cells by activating the PI3K/AKT signaling pathway,inhibits muscle ring finger 1(MuRF1)and atropin-1(Atrogin-1),induces skeletal muscle protein synthesis,and inhibits muscle atrophy.Exercise can effectively improve insulin resistance,activate PI3K/AKT signaling pathway cascade reaction,improve oxidative stress and reduce systemic low-grade inflammation.The activated PI3K/AKT signaling pathway can also protect skeletal muscle mitochondrial function,inhibit skeletal muscle mitochondrial oxidative stress and autophagy,increase skeletal muscle protein synthesis,and improve diabetes induced skeletal muscle atrophy.At the same time,exercise activated PI3K/AKT can up regulate VEGF,induce angiogenesis,promote vascular endothelial cell damage repair,improve skeletal muscle cell function in diabetes,and promote skeletal muscle growth.This article reviews the mechanism of exercise activating PI3K/AKT pathway to improve skeletal muscle atrophy in diabetes,aiming to provide theoretical basis for exercise to improve skeletal muscle atrophy in diabetes.关键词
糖尿病/骨骼肌萎缩/PI3K/AKT/运动Key words
diabetes/skeletal muscle atrophy/PI3K/AKT/exercise分类
社会科学引用本文复制引用
赵常红,王菲菲,连红强,王烨颖..运动改善糖尿病骨骼肌萎缩的研究进展与展望[J].天津体育学院学报,2025,40(3):322-330,9.基金项目
国家社会科学基金项目(项目编号:22BTY102) （项目编号:22BTY102）
西北师范大学运动与骨健康实验室建设项目(项目编号:6014202002100091) （项目编号:6014202002100091）
西北师范大学研究生培养与课程改革项目 （）
