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下丘脑神经肽对进食及体重的调节——瘦素作用的介导

Feeding and body-weight regulation by hypothalamic neuropeptides--mediation of the actions of leptin.

作者信息

Inui A

机构信息

Second Dept of Internal Medicine, Kobe University School of Medicine, Japan.

出版信息

Trends Neurosci. 1999 Feb;22(2):62-7. doi: 10.1016/s0166-2236(98)01292-2.

Abstract

Neuropeptides are essential for the regulation of appetite and body weight within the hypothalamus. The understanding of the neuropeptide regulation of energy homeostasis has been greatly advanced by the recent discovery of leptin, the protein product of the obese gene (ob). Significant new insights into the relationship between peripheral adiposity signals and their impact on the hypothalamic neuropeptide signaling circuitry have provided some crucial missing links in the negative-feedback regulation of appetite and body weight. The neuropeptide Y orexigenic network is a final common pathway for this signaling cascade and, along with feeding-inhibitory neuropeptides such as melanocortin, corticotropin-releasing factor and glucagon-like peptide 1, it is a major target through which leptin exerts a regulatory tonic restraint on body adiposity.

摘要

神经肽对于下丘脑内食欲和体重的调节至关重要。肥胖基因(ob)的蛋白质产物瘦素的近期发现,极大地推动了对神经肽调节能量稳态的理解。外周肥胖信号与其对下丘脑神经肽信号传导通路的影响之间关系的重大新见解,为食欲和体重的负反馈调节提供了一些关键的缺失环节。神经肽Y促食欲网络是该信号级联反应的最终共同途径,并且与诸如黑皮质素、促肾上腺皮质激素释放因子和胰高血糖素样肽1等抑制进食的神经肽一起,是瘦素对身体肥胖发挥调节性紧张性抑制作用的主要靶点。

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