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Ghrelin 和 GLP-1 之间的功能相互作用通过迷走传入系统调节进食。

Functional interaction between Ghrelin and GLP-1 regulates feeding through the vagal afferent system.

机构信息

Division of Neurology, Respirology, Endocrinology, and Metabolism, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, 889-1692, Japan.

Toronto General Hospital Research Institute, UHN, Toronto, ON, M5G 1L7, Canada.

出版信息

Sci Rep. 2020 Oct 28;10(1):18415. doi: 10.1038/s41598-020-75621-5.

DOI:10.1038/s41598-020-75621-5
PMID:33116243
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7595212/
Abstract

The gastrointestinal tract transmits feeding-regulatory signals to the brain via neuronal and hormonal pathways. Here we studied the interaction between the orexigenic gastric peptide, ghrelin, and the anorectic intestinal peptide, glucagon-like peptide 1 (GLP-1), in terms of feeding regulation via the vagal afferents. GLP-1 preadministration 30 min before ghrelin administration to rats and mice abolished ghrelin-induced food intake, while ghrelin preadministration abolished the anorectic effect of GLP-1. Ghrelin preadministration suppressed GLP-1-induced Fos expression in the nodose ganglia (NG). Electrophysiological assessment confirmed that the initially administered peptide abolished the vagal afferent electrical alteration induced by the subsequently administered peptide. Both the growth hormone secretagogue receptor (GHSR) and the GLP-1 receptor (GLP-1R) are co-localised in a major proportion of NG neurons that innervate the stomach. In these GhsrGlp1r neurons, ghrelin preadministration abolished the GLP-1-induced calcium response. Ghrelin generated a hyperpolarising current and GLP-1 generated a depolarising current in isolated NG neurons in a patch-clamp experiment. Ghrelin and GLP-1 potently influenced each other in terms of vagally mediated feeding regulation. This peptidergic interaction allows for fine control of the electrophysiological properties of NG neurons.

摘要

胃肠道通过神经元和激素途径将摄食调节信号传递到大脑。在这里，我们研究了摄食肽 ghrelin 和肠降血糖素肽 1 (GLP-1) 之间通过迷走传入神经相互作用的摄食调节。在大鼠和小鼠中，GLP-1 在 ghrelin 给药前 30 分钟给药可消除 ghrelin 诱导的摄食，而 ghrelin 给药可消除 GLP-1 的厌食作用。Ghrelin 给药可抑制 NG 中 GLP-1 诱导的 Fos 表达。电生理评估证实，最初给予的肽可消除随后给予的肽引起的迷走传入电变化。生长激素促分泌素受体 (GHSR) 和 GLP-1 受体 (GLP-1R) 均在支配胃的大部分 NG 神经元中共同定位。在这些 GhsrGlp1r 神经元中，ghrelin 给药可消除 GLP-1 诱导的钙反应。在膜片钳实验中，ghrelin 在分离的 NG 神经元中产生超极化电流，而 GLP-1 产生去极化电流。Ghrelin 和 GLP-1 强烈影响迷走神经介导的摄食调节。这种肽相互作用允许对 NG 神经元的电生理特性进行精细控制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b84/7595212/ba1d591c8e80/41598_2020_75621_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b84/7595212/77aab9aa3050/41598_2020_75621_Fig1a_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b84/7595212/33d352054b58/41598_2020_75621_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b84/7595212/1aec8c717340/41598_2020_75621_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b84/7595212/ba1d591c8e80/41598_2020_75621_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b84/7595212/77aab9aa3050/41598_2020_75621_Fig1a_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b84/7595212/33d352054b58/41598_2020_75621_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b84/7595212/1aec8c717340/41598_2020_75621_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b84/7595212/ba1d591c8e80/41598_2020_75621_Fig4_HTML.jpg

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