3-吲哚丙酸通过迷走神经调控动物采食的肠-脑轴机制  

Intestine-brain axis mechanism of 3-indolepropionic acid regulating animal feeding through vagus nerve

作　　者：朱琴 朱灿俊 江青艳[1] 郑斌 ZHU Qin;ZHU Canjun;JIANG Qingyan;ZHENG Bin(College of Animal Science,South China Agricultural University,Guangzhou 510642,China;Nanning Dabeinong Feed Technology Co.,Ltd.,Nanning 530105,China)

机构地区：[1]华南农业大学动物科学学院,广东广州510642 [2]南宁大北农饲料科技有限责任公司,广西南宁530105

出　　处：《江西农业大学学报》2024年第5期1289-1297,共9页Acta Agriculturae Universitatis Jiangxiensis

基　　金：国家自然科学基金项目(32372968、32102626、U21A20245-3);国家重点研发计划项目(2022YFD1300401)。

摘　　要：【目的】食欲是影响采食量的最重要因素,来自中枢和外周的多种信号经下丘脑食欲中枢感应和整合后调控采食,肠-脑轴在动物食欲调控中发挥重要作用。旨在揭示3-吲哚丙酸调控动物采食的肠-脑轴机制,对揭示缓解动物厌食具有参考价值。【方法】以21只8周龄C57BL/6J雄性小鼠为试验对象,通过灌服0,1,10 mg/kg3-吲哚丙酸,检测其对小鼠采食量和体增重的影响;并采用膈下迷走神经切除术、c-Fos免疫荧光和药物遗传学等技术,探究3-吲哚丙酸通过迷走神经介导的肠-脑轴调控动物采食的神经环路。【结果】(1)与对照组相比,灌服10 mg/kg 3-吲哚丙酸可显著提高小鼠3 h的采食量(P<0.05)和激活孤束核神经元(P<0.01)神经元兴奋性,化学遗传学抑制孤束核神经元可阻断3-吲哚丙酸促采食的作用;(2)3-吲哚丙酸抑制迷走传入神经兴奋性(P<0.001),膈下迷走神经切断或化学遗传学激活NG神经节均可消除3-吲哚丙酸促采食的作用。【结论】3-吲哚丙酸通过抑制肠道迷走传入神经兴奋性,从而激活孤束核神经元,提高动物采食量。[Objective]Appetite is the most important factor affecting feed intake,multiple signals from central and peripheral sources can regulate feeding via the hypothalamic appetite center,and the intestinebrain axis plays an important role in appetite regulation in animals.This study aims to reveal the mechanism of intestine-brain axis in mediating 3-indolepropionic acid in regulating feed intake of animals,which is of high reference value for improving feed intake of animals.[Method]Twenty one 8-week-old C57BL/6J male mice were used as test subjects.The effects of different concentrations of 3-indolepropionic acid and normal saline on feed intake and body weight gain of mice were detected and analyzed respectively.Subsequently,techniques such as subdiaphragmatic vagotomy,c-Fos immunofluorescence and pharmacogenetics were used to reveal the neural circuitry of 3-indolepropionic acid in regulating the excitability of neurons in the nucleus tractus solitarius via the vagus nerve.[Result](1)Compared with the control group,10 mg/kg of 3-indolepropionic acid significantly increased the feed intake of mice for 3 h(P<0.05);3-indolepropionic acid increased the feed intake of mice through the activation of solitary tract nucleus(SCTN)neurons(P<0.01),and chemogenetic inhibition of the SCTN neurons eliminated the feeding-promoting effect of 3-indolepropionic acid;(2)3-Indolepropionic acid activated NG neurons through intestinal vagus nerve(P<0.001).Subphrenic vagotomy or chemical genetic activation of NG ganglion could eliminate the effect of 3-Indolepropionic acid on food intake.[Conclusion]3-indolepropionic acid activates solitary tract nucleus neurons through intestinal vagal neurotransmission,thereby increasing food intake in animals.

关 键 词：采食调控 肠-脑轴 迷走传入神经 孤束核 3-吲哚丙酸 

分 类 号：S852.2[农业科学—基础兽医学]