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葡萄糖可逆转禁食诱导的小鼠弓状核激活。

Glucose reverses fasting-induced activation in the arcuate nucleus of mice.

作者信息

Becskei Csilla, Lutz Thomas A, Riediger Thomas

机构信息

Institute of Veterinary Physiology and Zurich Centre of Integrative Human Physiology, University of Zurich, Zurich, Switzerland.

出版信息

Neuroreport. 2008 Jan 8;19(1):105-9. doi: 10.1097/WNR.0b013e3282f380a2.

Abstract

The hypothalamic arcuate nucleus is an important target for metabolic and hormonal signals controlling food intake. As demonstrated by c-Fos studies, arcuate neurons are activated in food-deprived mice, whereas refeeding reverses the fasting-induced activation. To evaluate whether an increase in blood glucose has an inhibitory effect on these neurons, we analyzed the c-Fos response to an intraperitoneal glucose injection in fasted mice. This treatment increased blood glucose levels twofold and reduced 2-h food intake. Similar to refeeding, it also reversed the fasting-induced activation in the arcuate nucleus. Therefore, an increase in blood glucose might be an important feeding-related signal acting via the arcuate nucleus to oppose orexigenic stimuli.

摘要

下丘脑弓状核是控制食物摄入的代谢和激素信号的重要靶点。如c-Fos研究所示,饥饿小鼠的弓状神经元被激活,而重新进食可逆转禁食诱导的激活。为了评估血糖升高是否对这些神经元有抑制作用,我们分析了禁食小鼠腹腔注射葡萄糖后c-Fos的反应。这种处理使血糖水平增加了两倍,并减少了2小时的食物摄入量。与重新进食相似,它也逆转了弓状核中禁食诱导的激活。因此,血糖升高可能是一种重要的与进食相关的信号,通过弓状核发挥作用以对抗促食欲刺激。

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