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A unified model for the action of leptin on bone turnover
Author(s) -
Gordeladze Jan O.,
Reseland Janne E.
Publication year - 2003
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.10385
Subject(s) - leptin , osteoprotegerin , autocrine signalling , endocrinology , bone remodeling , medicine , osteoblast , chemistry , microbiology and biotechnology , biology , activator (genetics) , receptor , in vitro , biochemistry , obesity
Leptin has been advocated as a centrally acting factor responsible for inhibiting accumulation of bone mass. However, recent investigations unequivocally establish leptin as a local (autocrine) factor expressed by osteoblasts. Exogenously added leptin causes osteoblastic cell proliferation and differentiation, while also rendering osteoblasts more efficacious in terms of mineralization. Leptin acts as an anti‐apoptotic agent, and augments messages responsible for the remodelling of bone tissue, i.e., mRNAs for osteoprotegerin (OPG) and the interleukin IL‐6. Furthermore, leptin message is readily expressed in osteoblasts subjected to mechanical strain. In this respect, osteoblasts, which are unilaterally stretched proliferate and differentiate, a phenomenon being potentiated by exposure of the cells to differentiating humoral factors. This article discusses a unified model of dually acting leptin through the central nervous system and the mechanostat principle applied to osteoblasts. The proposed model may account for the finely tuned bone homeostasis maintained within rather narrow limits, depending on exposure to humoral factors and the prevailing mechanostat usage mode. © 2002 Wiley‐Liss, Inc.