康杰克葡萄甘通过抑制下丘脑炎症反应和神经元表达来抑制肥胖小鼠的食欲

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Hong Jin^1,2, Lanlan Yao^1,2, Wenjing Chen^1,2

¹College of Food Science and Technology, Huazhong Agricultural University, Wuhan 430070, China.

Journal of agricultural and food chemistry

|October 28, 2024

概括

康杰克葡萄甘 (KGM) 对肥胖和非肥胖小鼠的食欲有不同的影响. 在肥胖小鼠中,KGM抑制食欲和炎症,而在非肥胖小鼠中,它保持食欲,但通过肠-大脑轴增加炎症.

科学领域:

营养科学营养科学
神经科学是一个神经科学.
微生物组研究微生物组研究

背景情况:

康杰克葡萄甘 (KGM) 被公认为对食欲进行控制.
它通过下丘脑神经元和肠道微生物群调节食欲的精确机制,特别是在非肥胖个体中,需要进一步研究.

研究的目的:

研究KGM对肥胖小鼠和非肥胖小鼠食欲和能量代谢的影响.
探索下丘脑炎症,神经元基因表达和肠道微生物群在介导KGM影响中的作用.

主要方法:

在肥胖和非肥胖小鼠模型中对KGM对食物摄入量,能量消耗和下丘脑炎症的影响进行比较分析.
基因表达分析下丘脑食欲调节神经 (Agrp,Npy,Orx,Cart) 的基因表达.
肠道微生物群的分析和分析短链脂肪酸 (SCFA) 和脂胆水平.

主要成果:

在肥胖小鼠中,KGM减少了食物摄入量,下丘脑炎症和氧基因表达,同时增加了能量消耗和有益的肠道微生物群/SCFA.
在非肥胖小鼠中,KGM维持了食物摄入量和能量消耗,但加剧了下丘脑炎症,改变了特定的微生物种群.
KGM的效应与下丘脑神经元活动的变化,肠道微生物群组成,SCFA生产和酸丁胆水平的变化有关,这表明了个性化的反应.

结论:

在肥胖和非肥胖状态之间,KGM对食欲调节和能量代谢有不同的影响.
肠-大脑轴,涉及下丘脑炎症,神经元信号和KGM诱导的肠道微生物群调节,是这些差异效应的核心.
KGM对食欲和新陈代谢的影响是个性化的,强调考虑宿主状态 (肥胖或不肥胖) 和肠道微生物组合的重要性.

关键词:

胃口,食欲的增加.饮食纤维的食物纤维.我们的肠道微生物群.脑下垂体炎症性炎症是什么下丘脑中的神经元.康杰克葡萄康曼南 (glucomannan) 是一种葡萄糖.

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