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.
TITLE: PPAR-gamma insufficiency enhances osteogenesis through osteoblast formation from bone marrow progenitors.
AUTHOR CONTACT:
Hiroshi Kawaguchi
The University of Tokyo, Tokyo, Japan
Phone: 81-3-3815-5411 ext. 30473 or 33376
Fax: 81-3-3818-4082
E-mail: kawaguchi-ort@h.u-tokyo.ac.jp
View the PDF of this article at: http://www.jci.org/cgi/content/full/113/6/846
ACCOMPANYING COMMENTARY: Fat's loss is bone's gain
AUTHOR CONTACT:
Peter Tontonoz
University of California Los Angeles, Los Angeles, California, USA
Phone: 310-206-4546
Fax: 310-267-0382
E-mail: ptontonoz@mednet.ucla.edu
Journal
Journal of Clinical Investigation