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瘦素对骨骼与能量代谢的协同调节作用。

Leptin-dependent co-regulation of bone and energy metabolism.

作者信息

Yadav Vijay K, Karsenty Gerard

机构信息

Department of Genetics and Development, Columbia University Medical Centre, New York, NY 10032, USA.

出版信息

Aging (Albany NY). 2009 Nov 5;1(11):954-6. doi: 10.18632/aging.100100.

DOI:10.18632/aging.100100
PMID:20157577
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2815747/
Abstract

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.

摘要

脂肪细胞分泌的激素瘦素可抑制食欲并减少骨质累积。为实现这两种功能,瘦素需要下丘脑神经元的完整性,但并不依赖于这些神经元上其受体ObRb的表达。这些结果表明,瘦素首先在大脑的其他部位发挥作用来介导这些功能。然而,瘦素在大脑中的这个神经解剖学作用位点仍然难以捉摸。最近的小鼠遗传学、电生理学和神经解剖学研究提供了证据,表明瘦素通过一个两步途径抑制食欲和减少骨质累积:它减少脑干神经元中血清素的合成和释放,而血清素反过来作用于下丘脑神经元以调节食欲和骨质累积。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f70/2815747/18db28e73624/aging-01-954-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f70/2815747/18db28e73624/aging-01-954-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f70/2815747/18db28e73624/aging-01-954-g001.jpg

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Cell. 2009 Sep 4;138(5):976-89. doi: 10.1016/j.cell.2009.06.051.
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Lrp5 controls bone formation by inhibiting serotonin synthesis in the duodenum.Lrp5通过抑制十二指肠中血清素的合成来控制骨形成。
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Low bone mass in premenopausal women with depression.患有抑郁症的绝经前女性骨量低。
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瘦体重作为绝经后女性股骨近端骨密度的一个决定因素。
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Leptin induces osteocalcin expression in ATDC5 cells through activation of the MAPK-ERK1/2 signaling pathway.瘦素通过激活丝裂原活化蛋白激酶-细胞外信号调节激酶1/2(MAPK-ERK1/2)信号通路诱导ATDC5细胞中骨钙素的表达。
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