| Type 2 diabetes (T2DM) is associated with increased fracture risk. The mechanisms underlying skeletal fragility are multifactorial and likely include obesity, hyperglycaemia, oxidative stress, and accumulation of advanced glycation end products, leading to altered bone metabolism, structure, and strength. This article mainly explores the possible mechanisms of bone metabolism disorder of T2DM, including fat inflammation caused by excessive fat accumulation and T2DM related muscle atrophy. Recently, studies have found that sodium-glucose cotransporter 2 inhibitor (SGLT2i) may cause bone loss or increase fracture risk due to altered calcium, phosphate, and sodium concentration. This review explores that SGLT2i indirectly affects bone metabolism disorder of T2DM by affecting fat distribution, maintaining muscle mass, and reducing the inflammatory reaction of fat and muscle by reducing weight. Additionally, SGLT2i increases fracture risk more likely to be associated with falls and volume depletion secondary to osmotic diuresis in older patients with insufficient renal function and high cardiovascular risk. |