作者: Shu Takeda , Florent Elefteriou , Regis Levasseur , Xiuyun Liu , Liping Zhao
DOI: 10.1016/S0092-8674(02)01049-8
关键词:
摘要: We previously showed that leptin inhibits bone formation by an undefined mechanism. Here, we show hypothalamic leptin-dependent antiosteogenic and anorexigenic networks differ, the peripheral mediators of function appear to be neuronal. Neuropeptides mediating do not affect formation. Leptin deficiency results in low sympathetic tone, genetic or pharmacological ablation adrenergic signaling leads a leptin-resistant high mass. beta-adrenergic receptors on osteoblasts regulate their proliferation, agonist decreases mass leptin-deficient wild-type mice while antagonist increases ovariectomized mice. None these manipulations affects body weight. This study demonstrates neuronal regulation with potential therapeutic implications for osteoporosis.