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The bare bones of cutting the fat

Osteoporosis affects over 10 million individuals in the United States. The overall level of bone mass in an individual is known to be controlled primarily by the balance between the two cell types involved in bone remodeling: osteoblasts, which regenerate bone tissue, and osteoclasts, which degrade it.

Osteoblasts come from mesenchymal progenitor cells, which can also give rise to fat cells, called adipocytes. An intriguing fact is that in aging individuals while osteoblast development declines, there is an increase in the presence of adipocytes in the bone marrow.

In the March 15 issue of the Journal of Clinical Investigation, Hiroshi Kawaguchi and colleagues, from the University of Tokyo, investigate the relationship between the generation of bone-building cells and fat-storage cells, by looking at the effect of the loss of a protein called PPAR-gamma, a key regulator in adipocyte development, in mesenchymal cell differentiation into bone or fat cells.

Mice that were deficient in one of their PPAR-gamma genes had increased bone mass and a higher generation of osteoblasts. Furthermore, mouse embryonic stem (ES) cells that had no PPAR-gamma gene completely failed to differentiate into adipocytes, but spontaneously formed osteoblasts.

These and other data indicate an intriguing reciprocal relationship between bone and fat development, and may provide a new avenue for osteoporosis therapies.

In an accompanying commentary, Peter Tontonoz and Liming Pei, from the University of California in Los Angeles, discuss the findings of this study in the broader context PPAR-gamma's role in fat development as well as the strengths and limitations of likely use of the pathway for novel osteoporosis therapy.


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Contact: Laurie Goodman
lgoodman@the-jci.org
212-342-4159
Journal of Clinical Investigation
15-Mar-2004


Page: 1

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