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谷氨酸受体拮抗剂可抑制再喂养或葡萄糖给药后 nesfatin-1 神经元的激活。

Glutamate receptor antagonist suppresses the activation of nesfatin-1 neurons following refeeding or glucose administration.

机构信息

Department of Histology and Embryology, Balikesir University School of Medicine, Balikesir, Turkey.

Department of Histology and Embryology, Bursa Uludag University School of Medicine, Bursa, Turkey.

出版信息

Folia Morphol (Warsz). 2022;81(2):379-386. doi: 10.5603/FM.a2021.0034. Epub 2021 Mar 29.

DOI:10.5603/FM.a2021.0034
PMID:33778937
Abstract

BACKGROUND

Nesfatin-1 is a newly identified satiety peptide that has regulatory effects on food intake and glucose metabolism, and is located in the hypothalamic nuclei, including the supraoptic nucleus (SON). In this study, we have investigated the hypothesis that nesfatin-1 neurons are activated by refeeding and intraperitoneal glucose injection and that the glutamatergic system has regulatory influences on nesfatin-1 neurons in the SON.

MATERIALS AND METHODS

The first set of experiments analysed activation of nesfatin-1 neurons after refeeding as a physiological stimulus and the effectiveness of the glutamatergic system on this physiological stimulation. The subjects were randomly divided into three groups: fasting group, refeeding group and antagonist (CNQX + refeeding) group. The second set of experiments analysed activation of nesfatin-1 neurons by glucose injection as a metabolic stimulus and the effectiveness of the glutamatergic system on this metabolic stimulation. The subjects were randomly divided into three groups: saline group, glucose group and antagonist (CNQX + glucose) group.

RESULTS

Refeeding significantly increased the number of activated nesfatin-1 neurons by approximately 66%, and intraperitoneal glucose injection activated these neurons by about 55%, compared to the fasting and saline controls. The injections of glutamate antagonist (CNQX) greatly decreased the number of activated nesfatin-1 neurons.

CONCLUSIONS

This study suggested that nesfatin-1 neurons were activated by peripheral and/or metabolic signals and that this effect was mediated through the glutamatergic system.

摘要

背景

Nesfatin-1 是一种新发现的饱腹肽,对摄食和葡萄糖代谢有调节作用,位于下丘脑核,包括视上核(SON)。在这项研究中,我们假设 nesfatin-1 神经元被再喂养和腹腔内葡萄糖注射激活,并且谷氨酸能系统对 SON 中的 nesfatin-1 神经元具有调节作用。

材料和方法

第一组实验分析了再喂养作为生理刺激时 nesfatin-1 神经元的激活情况,以及谷氨酸能系统对这种生理刺激的有效性。将实验对象随机分为三组:禁食组、再喂养组和拮抗剂(CNQX+再喂养)组。第二组实验分析了葡萄糖注射作为代谢刺激时 nesfatin-1 神经元的激活情况,以及谷氨酸能系统对这种代谢刺激的有效性。将实验对象随机分为三组:盐水组、葡萄糖组和拮抗剂(CNQX+葡萄糖)组。

结果

与禁食和盐水对照组相比,再喂养显著增加了约 66%的激活 nesfatin-1 神经元的数量,而腹腔内葡萄糖注射则使这些神经元激活约 55%。谷氨酸拮抗剂(CNQX)的注射大大减少了激活的 nesfatin-1 神经元的数量。

结论

本研究表明,nesfatin-1 神经元被外周和/或代谢信号激活,这种作用是通过谷氨酸能系统介导的。

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