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HERO ID
515944
Reference Type
Journal Article
Title
Mechanisms of disease: is osteoporosis the obesity of bone?
Author(s)
Rosen, CJ; Bouxsein, ML
Year
2006
Is Peer Reviewed?
1
Journal
Nature Clinical Practice Rheumatology
ISSN:
1745-8382
EISSN:
1745-8390
Volume
2
Issue
1
Page Numbers
35-43
Language
English
DOI
10.1038/ncprheum0070
Abstract
Osteoporosis and obesity, two disorders of body composition, are growing in prevalence. Interestingly, these diseases share several features including a genetic predisposition and a common progenitor cell. With aging, the composition of bone marrow shifts to favor the presence of adipocytes, osteoclast activity increases, and osteoblast function declines, resulting in osteoporosis. Secondary causes of osteoporosis, including diabetes mellitus, glucocorticoids and immobility, are associated with bone-marrow adiposity. In this review, we ask a provocative question: does fat infiltration in the bone marrow cause low bone mass or is it a result of bone loss? Unraveling the interface between bone and fat at a molecular and cellular level is likely to lead to a better understanding of several diseases, and to the development of drugs for both osteoporosis and obesity.
Keywords
adipocyte; bone; fat; obesity; osteoporosis; sympathetic-nervous-system; proton mr spectroscopy; receptor ko mice; mineral density; marrow stroma; adipogenic differentiation; osteoblast; differentiation; postmenopausal women; leptin deficiency; body-composition
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