Research indicates that AT indirectly inhibits MSTN expression by modulating endocrine functions (such as lowering blood glucose and insulin levels) and enhancing energy expenditure, which reduces fat accumulation and alleviates systemic inflammation and insulin resistance, thereby promoting glucose uptake by skeletal muscles and insulin secretion by the pancreas, ultimately improving bone metabolism disorders in T2DM patients [153,156]. This evidence concerns the gene MSTN and metabolic bone disorder.