Fat's loss is bone's gain

Abstract

Osteoporosis, characterized by low bone mass and structural deterioration of bone tissue with an increased susceptibility to fractures, is a major public health threat to the elderly. Bone mass homeostasis in adults is maintained locally by the balance between osteoblastic bone formation and osteoclastic bone resorption. Haploinsufficiency of PPARgamma, a key transcription factor implicated previously in adipogenesis, lipid metabolism, and glucose homeostasis, has now been shown to promote osteogenesis through enhanced osteoblast formation. These findings support a reciprocal relationship between the development of bone and fat, and may prompt further exploration of the PPAR pathway as a potential target for intervention in osteoporosis.

Figure 1

Model for the influence of the PPARγ pathway on osteogenesis. Bone homeostasis is maintained by the balance between osteoblastic bone formation and osteoclastic bone resorption. An imbalance between the two is associated with osteoporosis. The PPARγ pathway not only determines adipocyte differentiation from mesenchymal progenitors, but also inhibits osteoblast differentiation, as revealed by Akune et al. (10). This new finding raises the possibility of interrupting the PPARγ pathway for the treatment of osteoporosis.