Effects of Different Exercise Modes and Intensities on Skeletal Muscle Mammalian Target of Rapamycin Signaling in Strepto-zotocin and High-Fat-Diet Induced Prediabetic Mice

摘要

One of the notable characteristics of diabetes is atrophy of skeletal muscle fibers, which is a result of increased proteolysis, decreased protein synthesis, and decreased regenerative ability of damaged skeletal muscle (1,2). In diabetes, skeletal muscles show decreased expression of mammalian target of rapamycin (mTOR), involved in the process of muscle fiber growth and regeneration through muscle fiber and cell proliferation and differentiation, suggesting that the decreased function of mTOR can induce muscle fiber damage and dissolution due to suppression of muscle fiber proliferation and differentiation (2,3). Diabetes-induced rats through 3-day streptozotocin (STZ) treatment showed decreased protein synthesis within skeletal muscles to 60% and decreased mTOR expression to 36%, proving that skeletal muscle atrophy in diabetes stems from decreased mTOR expression (1).