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通过不同的回路抑制由炎症引起的厌恶和食物摄入

Haley S Province^1,2,3, Nikolas W Hayes^1,2, Nathan A Leong⁴

¹Department of Medicine, Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern University, Chicago, IL 60611, USA.

bioRxiv : the preprint server for biology

|August 20, 2025

概括

葡萄糖依赖的胰岛素多 (GIP) 受体激应减少了食物摄入量和厌恶. GIPR信号对厌食症和厌食症的不同神经回路产生影响,为炎症诱导的厌食症治疗提供了潜力.

科学领域:

神经科学
内分泌学
代谢过程

背景情况:

葡萄糖依赖性胰岛素多 (GIP) 是一种能调节能量恒温的隐形激素.
中心GIP受体 (GIPR) 的药理向显示了管理能量平衡和厌恶的潜力.
连接GIPR信号与食物摄入和厌恶的确切机制尚不清楚.

研究的目的:

调查GIPR激素对食物摄入和厌恶的影响的机制.
确定特定神经回路在GIPR中介作用.
探索GIPR激应作为炎症诱导的治疗策略.

主要方法:

使用GIPR激素与促炎性细胞因特鲁金-1β (IL-1β) 结合.
研究了与素基因相关的神经元 (CGRP) 在厌食症和厌食症中的参与.
检查了GIPR在背部阴道综合体中的作用,以发现厌食和抗厌食作用.

主要成果:

GIPR激素消除了IL-1β诱导的厌恶,并增强了它的厌食效应.
对IL-1β诱导的条件性味道回避而不是厌食症而言,双臂CGRP神经元是必不可少的.
系统性IL- 1β增加了CGRP神经活动,这种效应被GIPR激动剂的同时使用减弱了.
背部虚综合体中的GIPR引起了急性厌食症,但没有GIPR激素的抗厌食作用.

结论:

通过独特的神经通路减少食物摄入并防止厌恶.
背部虚综合体中的GIPR信号对于GIPR的厌食效应至关重要.
GIPR激应是一种有前途的治疗途径,可以缓解炎症引起的厌恶.

关键词:

CGRP神经元美国国际贸易委员会没有食欲有条件的味道回避炎症的发生疾病行为

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