Leptin-dependent co-regulation of bone and energy metabolism.
Leptin-dependent co-regulation of bone and energy metabolism.
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DOI：
10.18632/aging.100100
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发表时间：
2009-11-05
期刊：
影响因子：
--
通讯作者：
Karsenty G
中科院分区：
文献类型：
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作者：
Yadav VK;Karsenty G
的 脂肪细胞衍生的激素瘦素抑制食欲和骨量增加。 为了实现这两个功能，瘦素需要完整的 下丘脑神经元，但不表达其受体，ObRb对这些 神经元这些结果表明，瘦素首先在细胞的其他部位起作用。 大脑来调节这些功能。然而，这个神经解剖部位 瘦素在大脑中的作用仍然难以捉摸。最近的老鼠遗传学， 电生理学和神经解剖学研究提供了证据， 瘦素通过两步途径抑制食欲和骨量增加： 它会减少脑干神经元合成和释放血清素 反过来又作用于下丘脑神经元来调节食欲和骨骼 大量应计。
The adipocyte-derived hormone leptin inhibits appetite and bone mass accrual. To fulfill these two functions leptin requires the integrity of hypothalamic neurons but not the expression of its receptor, ObRb on these neurons. These results suggested that leptin acts first elsewhere in the brain to mediate these functions. However, this neuroanatomical site of leptin action in the brain remained elusive. Recent mouse genetic, electrophysiological and neuroanatomical studies provide evidence that leptin inhibits appetite and bone mass accrual through a two-step pathway: it decreases synthesis and the release by brainstem neurons of serotonin that in turn targets hypothalamic neurons to regulate appetite and bone mass accrual.