运动如何改善糖尿病血糖？MSTN-AMPK/PGC-1α信号通路机制解析

Exercise intervention is considered a core strategy in the management of type 2 diabetes mellitus (T2DM) due to its safety and multi-target regulation advantages. However, the specific molecular mechanisms by which it improves skeletal muscle glucose metabolism have not been fully elucidated. Mitochondria, as the "powerhouses" of cells, may serve as a crucial link between exercise intervention and glucose metabolism through their quality control systems. Studies have shown that myokines secreted by skeletal muscle, such as myostatin (MSTN), may mediate the effects of exercise on systemic glucose homeostasis, with MSTN inhibition improving glucose tolerance. However, whether exercise regulates mitochondrial quality control by downregulating MSTN expression to improve glucose metabolism in T2DM skeletal muscle remains to be further verified. This study aims to investigate the effects of exercise interventions (moderate-intensity continuous training, MICT, and high-intensity interval training, HIIT) on glucose metabolism in the skeletal muscle of T2DM mice and to elucidate the underlying molecular mechanisms, with a focus on the regulatory role of the MSTN-AMPK/PGC-1α signaling pathway.