A possible link between BDNF and mTOR in control of food intake.
A possible link between BDNF and mTOR in control of food intake.
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DOI：
10.3389/fpsyg.2014.01093
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发表时间：
2014
影响因子：
3.8
通讯作者：
Nawa H
中科院分区：
文献类型：
--
作者：
Takei N;Furukawa K;Hanyu O;Sone H;Nawa H
食物的摄入量是由葡萄糖、氨基酸、激素、神经肽和营养因子通过下丘脑的神经回路复杂地调节的。脑源性神经营养因子(BDNF)是大脑中最重要的神经营养因子，在整个生命过程中调节着分化、成熟和突触的可塑性。在它的众多作用中，BDNF在大脑中发挥着厌食功能。然而，BDNF诱导的细胞内信号转导控制食物摄入的机制还不完全清楚。参与转导BDNF厌氧活性的分子之一是雷帕霉素的哺乳动物靶点(MTOR)。MTOR感知细胞外氨基酸、葡萄糖、生长因子和神经递质，并调节合成代谢反应对这些信号的反应。激活的mTOR增加蛋白质和脂肪的合成，并抑制蛋白质的降解。在下丘脑，mTOR的激活被认为会减少食物的摄入量。在这里，我们总结了关于BDNF和mTOR介导的摄食控制的最新发现，并提出了这些分子与进食行为之间的联系。
Food intake is intricately regulated by glucose, amino acids, hormones, neuropeptides, and trophic factors through a neural circuit in the hypothalamus. Brain-derived neurotrophic factor (BDNF), the most prominent neurotrophic factor in the brain, regulates differentiation, maturation, and synaptic plasticity throughout life. Among its many roles, BDNF exerts an anorexigenic function in the brain. However, the intracellular signaling induced by BDNF to control food intake is not fully understood. One candidate for the molecule involved in transducing the anorexigenic activity of BDNF is the mammalian target of rapamycin (mTOR). mTOR senses extracellular amino acids, glucose, growth factors, and neurotransmitters, and regulates anabolic reactions response to these signals. Activated mTOR increases protein and lipid synthesis and inhibits protein degradation. In the hypothalamus, mTOR activation is thought to reduce food intake. Here we summarize recent findings regarding BDNF- and mTOR-mediated feeding control, and propose a link between these molecules in eating behavior.
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