Thiazolidinediones on PPARγ: The Roles in Bone Remodeling

Figure 1

Potential mechanisms for TZD-induced bone loss. In vivo studies in both clinical trials and using animal models demonstrate that TZDs, a class of diabetic drugs that functions as PPARγ agonists, cause bone loss and increased fracture risk, especially in postmenopausal women, by simultaneously inhibiting bone formation and stimulating bone resorption. In addition to the well-documented direct effects of TZDs on bone cell differentiation and function, emerging evidence indicate that TZD may also exert its detrimental skeletal effects via several potential indirect effects, which provokes further investigation in future preclinical and clinical studies.