Accumulative evidence shows that type 2 diabetes patients have high fracture rate in spite of the absence of bone mineral density (BMD) reduction. The etiology and treatment of diabetes-related bone disease have recently attracted widespread attention. Recent epidemiologic studies have shown that the fracture rate was decreased in patients treated with metformin, one of the anti-hyperglycemic agents by improving insulin resistance. Several studies have indicated that metformin directly stimulated the differentiation of osteoblastic cells, and that metformin reversed deleterious effects of advanced glycation end products on these cells. Further longitudinal studies are needed to clarify the effects of metformin on BMD, bone turnover markers, and fracture risks in type 2 diabetes.