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A new oxytocin-saporin cytotoxin for lesioning oxytocin-receptive neurons in the rat hindbrain.一种新型的催产素-匙孔嘁血蓝蛋白细胞毒素,用于损伤大鼠后脑的催产素受体神经元。
Endocrinology. 2010 Sep;151(9):4207-13. doi: 10.1210/en.2010-0295. Epub 2010 Jul 7.
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Endogenous leptin signaling in the caudal nucleus tractus solitarius and area postrema is required for energy balance regulation.尾侧孤束核和迷走神经背核中的内源性瘦素信号对于能量平衡调节是必需的。
Cell Metab. 2010 Jan;11(1):77-83. doi: 10.1016/j.cmet.2009.10.009.
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Gastrin-releasing peptide messenger ribonucleic acid expression in the hypothalamic paraventricular nucleus is altered by melanocortin receptor stimulation and food deprivation.胃泌素释放肽信使核糖核酸在下丘脑室旁核中的表达会因黑皮质素受体刺激和食物剥夺而改变。
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Leptin regulation of the anorexic response to glucagon-like peptide-1 receptor stimulation.瘦素对胰高血糖素样肽-1受体刺激所致厌食反应的调节作用。
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Leptin modulation of peripheral controls of meal size.瘦素对进食量外周控制的调节作用。
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Leptin enhances feeding suppression and neural activation produced by systemically administered bombesin.瘦素增强了由全身注射蛙皮素所产生的摄食抑制和神经激活作用。
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Leptin action in the forebrain regulates the hindbrain response to satiety signals.瘦素在前脑的作用调节后脑对饱腹感信号的反应。
J Clin Invest. 2005 Mar;115(3):703-10. doi: 10.1172/JCI22081.
8
Evidence that paraventricular nucleus oxytocin neurons link hypothalamic leptin action to caudal brain stem nuclei controlling meal size.室旁核催产素神经元将下丘脑瘦素作用与控制进食量的脑桥尾侧核相连的证据。
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Cholecystokinin-mediated suppression of feeding involves the brainstem melanocortin system.胆囊收缩素介导的摄食抑制涉及脑干黑皮质素系统。
Nat Neurosci. 2004 Apr;7(4):335-6. doi: 10.1038/nn1214. Epub 2004 Mar 14.
10
Oxytocin innervation of caudal brainstem nuclei activated by cholecystokinin.胆囊收缩素激活的脑干尾端核团的催产素神经支配。
Brain Res. 2003 Dec 12;993(1-2):30-41. doi: 10.1016/j.brainres.2003.08.036.

肥胖信号与进餐量控制。

Adiposity signaling and meal size control.

机构信息

Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

出版信息

Physiol Behav. 2011 Apr 18;103(1):21-4. doi: 10.1016/j.physbeh.2010.11.013. Epub 2010 Nov 24.

DOI:10.1016/j.physbeh.2010.11.013
PMID:21110992
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3073578/
Abstract

Signaling from energy stores provides feedback on overall nutrient availability to influence food intake. Beginning with seminal studies by Woods and colleagues identifying insulin as an adiposity signal, it has become clear that such factors affect food intake by modulating the efficacy of within meal feedback satiety signals. More recent work with leptin has revealed actions of the hormone in modulating the efficacy of multiple gut feedback signals, identified the dorsal hindbrain as a site of signal integration and suggested both local and descending hypothalamic to hindbrain actions in mediating these effects. The original work by Woods and colleagues provided the necessary experimental paradigms for these advances.

摘要

能量储存的信号反馈对整体营养供应情况,从而影响食物摄入。从 Woods 及其同事最初的研究确定胰岛素作为肥胖信号开始,人们已经清楚地认识到,这些因素通过调节餐后反馈饱腹感信号的效率来影响食物摄入。最近关于瘦素的研究揭示了该激素在调节多种肠道反馈信号效率方面的作用,确定了背侧后脑作为信号整合的部位,并提出了局部和下行下丘脑到后脑的作用来介导这些效应。Woods 及其同事的最初研究为这些进展提供了必要的实验范例。