Resolving the Two “Bony” Faces of PPAR-γ
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...
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| Main Authors: | , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2006-01-01
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| Series: | PPAR Research |
| Online Access: | http://dx.doi.org/10.1155/PPAR/2006/27489 |
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| Summary: | 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. |
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| ISSN: | 1687-4757 1687-4765 |