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Submitted on November 22, 2004
Accepted on April 14, 2005
INSERM E0366, University Hospital of St-Etienne, France; INSERM U418, Lyon, France
* To whom correspondence should be addressed. E-mail: thierry.thomas{at}univ-st-etienne.fr.
In vitro studies have demonstrated leptin positive effects on the osteoblast lineage and negative effects on osteoclastogenesis. Therefore, we tested the hypothesis that leptin may prevent tail-suspension induced bone loss characterized by an uncoupling pattern of bone remodeling, through both mechanisms. Female rats were randomly tail-suspended or not and treated either with intraperitoneal administration of leptin or vehicle for 3, 7 and 14 days. As measured by DXA, tail-suspension induced a progressive decrease in tibia-metaphysis BMD, which was prevented by leptin. Histomorphometry showed that this was related to the prevention of the transient increase in osteoclast number observed with suspension at D7. These effects could be mediated by the RANK-ligand (RANKL)/osteoprotegerin (OPG) pathway since we observed using direct RT-PCR, a suspension-induced increase in RANK-L gene expression in proximal tibia at D3, which was counterbalanced by leptin administration with a similar 3-fold increase in OPG expression and an RANK-L/OPG ratio close to non-suspended conditions. In addition, leptin prevented the decrease in bone formation rate induced by tail-suspension at D14. The latter could be related to leptin role in mediating the reciprocal differentiation between adipocytes and osteoblasts since leptin concurrently blunted the disuse-induced increase in bone marrow adipogenesis. In summary, these data suggest that peripheral administration of leptin could prevent disuse-induced bone loss through first a major inhibitory effect on bone resorption and second a delayed effect preventing the decrease in bone formation.
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