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PPAR Research
Volume 2006, Article ID 27489, 9 pages
Review Article

Resolving the Two “Bony” Faces of PPAR-γ

1Department of Geriatrics, Reynolds Institute on Aging, University of Arkansas for Medical Sciences, 629 Jack Stephens Drive, Little Rock, AR 72205, USA
2Department of Orthopaedic Surgery, Center for Orthopaedic Research, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA

Received 31 May 2006; Revised 18 July 2006; Accepted 19 July 2006

Copyright © 2006 Beata Lecka-Czernik and Larry J. Suva. 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.


Bone loss with aging results from attenuated and unbalanced bone turnover that has been associated with a decreased number of bone forming osteoblasts, an increased number of bone resorbing osteoclasts, and an increased number of adipocytes (fat cells) in the bone marrow. Osteoblasts and adipocytes are derived from marrow mesenchymal stroma/stem cells (MSC). The milieu of intracellular and extracellular signals that controls MSC lineage allocation is diverse. The adipocyte-specific transcription factor peroxisome proliferator-activated receptor-gamma (PPAR-γ) acts as a critical positive regulator of marrow adipocyte formation and as a negative regulator of osteoblast development. In vivo, increased PPAR-γ activity leads to bone loss, similar to the bone loss observed with aging, whereas decreased PPAR-γ activity results in increased bone mass. Emerging evidence suggests that the pro-adipocytic and the anti-osteoblastic properties of PPAR-γ are ligand-selective, suggesting the existence of multiple mechanisms by which PPAR-γ controls bone mass and fat mass in bone.