PPAR Research
Volume 2006 (2006), Article ID 24502, 6 pages
doi:10.1155/PPAR/2006/24502
Review Article

Diabetes, TZDs, and Bone: A Review of the Clinical Evidence

Ann V. Schwartz

Department of Epidemiology and Biostatistics, University of California, San Francisco, 185 Berry Street, Suite 5700, San Francisco 94107, CA, USA

Received 1 April 2006; Revised 7 July 2006; Accepted 10 July 2006

Copyright © 2006 Ann V. Schwartz. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Evidence from rodent and in vitro models suggests that activation of PPAR-γ by thiazolidinediones (TZDs) causes increased bone marrow adiposity and decreased osteoblastogenesis, resulting in bone loss. TZDs are prescribed for the treatment of diabetes, providing an opportunity to determine whether PPAR-γ activation also impacts bone in humans. In addition, since type 2 diabetes is associated with higher fracture risk, an understanding of the clinical impact of TZDs on bone is needed to guide fracture prevention efforts in this population. This review summarizes current findings regarding type 2 diabetes and increased fracture risk and then considers the available evidence regarding TZD use and bone metabolism in humans.