期刊
NEURON
卷 49, 期 2, 页码 191-203出版社
CELL PRESS
DOI: 10.1016/j.neuron.2005.12.021
关键词
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资金
- NIDDK NIH HHS [DK53301, R01 DK53301-07S2, 5T32DK07516, 1F32DK64564-01, P01 DK56116] Funding Source: Medline
- NIMH NIH HHS [MH61583] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
Leptin, an adipocyte-derived hormone, acts directly on the brain to control food intake and energy expenditure. An important question is the identity of first-order neurons initiating leptin's anti-obesity effects. A widely held view is that most, if not all, of leptin's effects are mediated by neurons located in the arcuate nucleus of the hypothalamus. However, leptin receptors (LEPRs) are expressed in other sites as well, including the ventromedial hypothalamus (VMH). The possible role of leptin acting in nonarcuate sites has largely been ignored. In the present study, we show that leptin depolarizes and increases the firing rate of steroidogenic factor-1 (SF1)-positive neurons in the VMH. We also show, by generating mice that lack LEPRs on SF1-positive neurons, that leptin action at this site plays an important role in reducing body weight and, of note, in resisting diet-induced obesity. These results reveal a critical role for leptin action on VMH neurons.
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