Bone mass is maintained constant between puberty and menopause by the balance between osteoblast and osteoclast activity. The existence of a hormonal control of osteoblast activity has been speculated for years by analogy to osteoclast biology. Through the search for such humoral signal(s) regulating bone formation, leptin has been identified as a strong inhibitor of bone formation. Furthermore, intracerebroventricular infusion of leptin has shown that the effect of this adipocyte-derived hormone on bone is mediated via a brain relay. Subsequent studies have led to the identification of hypothalamic groups of neurons involved in leptin's antiosteogenic function. In addition, those neurons or neuronal pathways are distinct from neurons responsible for the regulation of energy metabolism. Finally, the peripheral mediator of leptin's antiosteogenic function has been identified as the sympathetic nervous system. Sympathomimetics administered to mice decreased bone formation and bone mass. Conversely, beta-blockers increased bone formation and bone mass and blunted the bone loss induced by ovariectomy.

中文翻译：

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常见的内分泌控制体重，生殖和骨量。

通过成骨细胞和破骨细胞活性之间的平衡，青春期和绝经之间的骨量保持恒定。类似于破骨细胞生物学已经推测了激素控制成骨细胞活性的存在已有多年。通过寻找调节骨形成的这种体液信号，瘦蛋白已被鉴定为骨形成的强抑制剂。此外，脑室内注射瘦素已经表明，这种脂肪细胞源性激素对骨骼的作用是通过脑中继介导的。随后的研究导致确定了瘦素的抗成骨功能的下丘脑神经元组。另外，那些神经元或神经元途径不同于负责能量代谢调节的神经元。最后，瘦素的外周介质 抗骨生成功能已被确定为交感神经系统。给小鼠施用的拟交感神经药减少了骨形成和骨量。相反，β受体阻滞剂增加了骨形成和骨量，并抑制了卵巢切除术引起的骨质流失。