Safety of antidiabetic therapies on bone

Abstract

Osteoporosis and diabetic disease have reached epidemic proportion and create significant public health concerns. The prevalence of these diseases is alarming, and indicates that in the United States, 50 % of elderly individuals are osteoporotic and almost 20 % of population has either diabetic or prediabetic conditions (Centers for Disease Control and Prevention; http://www.cdc.gov Osteoporosis and diabetes share many features including genetic predispositions and molecular mechanisms. Bone and energy homeostasis are under the control of the same regulatory factors, including peroxisome proliferator-activated receptor gamma (PPARγ), insulin, amylin, and gastrointestinal hormones. These factors and related mechanisms control glucose homeostasis and fatty acids metabolism in fat tissue, pancreas and intestine, which are pharmacological targets for antidiabetic therapies. The same factors contribute to the bone quality by their effect on bone cell differentiation and bone remodeling process. This implies that bone should be considered as a vital target for therapies which modulate energy metabolism and explains why certain antidiabetic therapies may affect bone.