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人参衍生GABAFG通过调节自-溶酶体通路和肠道微生物群来改善2型糖尿病

Meng-Han Qi¹, Hai-Yan Zhang¹, Yun-Yi Hou¹

¹College of Chinese Medicinal Materials, Jilin Provincial International Joint Research Center for the Development and Utilization of Authentic Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.

Journal of advanced research

|January 6, 2025

概括

人参衍生 γ-氨基黄油酸-果糖糖 (GABAFG) 通过改善葡萄糖和脂质代谢,有效治疗2型糖尿病 (T2DM). GABAFG保护胰腺细胞并积极改变肠道微生物群,为T2DM管理提供了一种新方法.

科学领域:

代谢性疾病研究研究.
药理学机制药理学机制
自然产品化学自然产品化学

背景情况:

2型糖尿病 (T2DM) 具有高血糖和高脂血症的特征,其来源于胰岛素抵抗和胰腺β细胞功能障碍.
人参 (Panax人参) 显示T2DM的治疗潜力,但其精确的机制仍然难以捉摸.

研究的目的:

为了研究治疗T2DM的治疗作用和γ-aminobutyric acid-fructosyl-glucose (GABAFG) 的潜在机制,这是一个来自人参的Maillard反应产物.
阐明GABAFG如何影响T2DM的背景下胰腺β细胞,胰岛素抵抗和肠道微生物群.

主要方法:

在血清和组织中分析GABAFG代谢,使用超高性能液态染色学-Q精确质谱法 (UHPLC-QE-MS).
研究了GABAFG在胰腺β细胞 (体外和体内) 中的分子机制,通过西方斑点,qPCR和免疫光.
使用高通量测序和血清代谢学验证的结果.

主要成果:

在高脂肪饮食/链毒素诱导的T2DM小鼠中,GABAFG治疗缓解了高血糖和高脂血症.
通过向胰腺β细胞中的IRS-1信号轴,GABAFG降低了胰岛素耐药性,并通过通过TFEB核转位来增强自细胞酶功能来抑制细胞亡.
GABAFG调节了肠道微生物群,增加了阿克尔曼西亚和减少了罗姆布茨亚,同时降低了血清葡萄糖脂代谢,以对抗T2DM诱导的脂质不良症.

结论:

这项研究首次评估了人参衍生GABAFG在T2DM中的药理作用.
这些发现为了解人参在代谢疾病中的有效性提供了一个新的理论框架.
通过解决多种病理途径,GABAFG为T2DM提供了一个有前途的治疗剂.

关键词:

自自是一种自的过程.在 GABAFGG 的基础上,GABAFG 人参就是一个人,人参就是一个人.我们的肠道微生物群.血清中的代谢产物 2型糖尿病是什么? 2型糖尿病是什么?

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