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PI3K signaling in the ventromedial hypothalamic nucleus is required for normal energy homeostasis.

机译:正常能量稳态需要腹侧下丘脑核中的PI3K信号传导。

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Phosphatidyl inositol 3-kinase (PI3K) signaling in the hypothalamus has been implicated in the regulation of energy homeostasis, but the critical brain sites where this intracellular signal integrates various metabolic cues to regulate food intake and energy expenditure are unknown. Here, we show that mice with reduced PI3K activity in the ventromedial hypothalamic nucleus (VMH) are more sensitive to high-fat diet-induced obesity due to reduced energy expenditure. In addition, inhibition of PI3K in the VMH impaired the ability to alter energy expenditure in response to acute high-fat diet feeding and food deprivation. Furthermore, the acute anorexigenic effects induced by exogenous leptin were blunted in the mutant mice. Collectively, our results indicate that PI3K activity in VMH neurons plays a physiologically relevant role in the regulation of energy expenditure.
机译:下丘脑中的磷脂酰肌醇3-激酶(PI3K)信号传导与能量稳态的调节有关,但该细胞内信号整合各种代谢线索以调节食物摄入和能量消耗的关键脑部位尚不清楚。在这里,我们显示在腹侧下丘脑核(VMH)中PI3K活性降低的小鼠由于能量消耗减少,对高脂饮食诱导的肥胖更为敏感。此外,对VMH中PI3K的抑制会削弱响应急性高脂饮食喂养和食物匮乏而改变能量消耗的能力。此外,在突变小鼠中,外源性瘦素诱导的急性厌食作用减弱。总体而言,我们的结果表明,VMH神经元中的PI3K活性在能量消耗的调节中起着生理相关的作用。

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