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在糖尿病脑病症中发现和功能验证肠道微生物群-代谢物-miRNA轴

Haitian Sun¹, Jingzhi Liu², Yanxiao Jing¹

¹Department of Endocrinology, The Second Affiliated Hospital of Shandong First Medical University, Taian 271000, China.

Archives of biochemistry and biophysics

|February 6, 2026

概括

糖尿病脑病变 (DE) 涉及肠道微生物群的变化和代谢变化,通过miR-493-3p/RAF1通路损害神经元. 这一发现为严重的糖尿病并发症DE提供了新的治疗点.

科学领域:

神经科学是一个神经科学.
微生物学微生物学
代谢学代谢学代谢学

背景情况:

糖尿病脑病变 (DE) 是糖尿病的一种严重的神经并发症,导致认知能力下降和神经元损伤.
肠道微生物群失调与糖尿病有关,但其在DE病原发生中的作用尚不清楚.

研究的目的:

研究肠道微生物群和代谢改变在糖尿病脑病变中的作用.
阐明DE中神经元损伤背后的分子机制.

主要方法:

在DE患者和糖尿病对照的便样本上使用了一种多omics方法 (16S rRNA测序和代谢学).
建立了一个体外DE模型,其中使用了高葡萄糖处理的细胞和来自DE患者的便微生物群.
评估了神经损伤标志物和miR-493-3p表达,并验证了miR-493-3p/RAF1相互作用.

主要成果:

DE患者表现出明显的肠道微生物组成和改变的代谢物概况,富含氨基酸和脂质代谢.
来自DE患者的便微生物群超级生物在体外加剧了高葡萄糖诱导的神经元损伤和亡.
观察到miR-493-3p的上调,其抑制通过恢复RAF1表达来保护神经元,确认RAF1是中介神经元损伤的目标.

结论:

在DE中,一种新的肠-大脑轴路径涉及肠道微生物群的失调和代谢变化,通过miR-493-3p/RAF1信号轴促进神经元损伤.
这些发现提供了对DE病原体的新见解.
已经确定了DE的潜在治疗点.

关键词:

糖尿病脑病变 - 糖尿病脑病变我们的肠道微生物群.肠-大脑轴肠-大脑轴代谢生物组的代谢生物组在 miR-493-3p 中使用.

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