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在小鼠中,肠道微生物群及其代谢物促进了患有糖尿病的疼痛性外围神经病变,并与认知功能障碍相复杂
Junpeng Yang1,2,3, Xin Lv3, Ya Xu1
1Department of Endocrinology, Henan Provincial Key Medicine Laboratory of Intestinal Microecology and Diabetes, Henan Provincial People's Hospital, Zhengzhou, Henan, China.
Frontiers in cellular and infection microbiology
|September 18, 2025
概括
肠道微生物群和代谢物与糖尿病小鼠的疼痛性糖尿病外围神经病变 (PDPN) 和认知障碍有关. 特定细菌和代谢物 (如Dl-乳酸盐) 的变化可能会导致这些疾病,这表明新的治疗点.
科学领域:
- 微生物学 微生物学
- 神经科学是一个神经科学.
- 代谢学 代谢学 代谢学
背景情况:
- 疼痛性糖尿病外围神经病变 (PDPN) 通常伴随着认知功能障碍.
- 肠道微生物群在糖尿病神经病变中的作用是公认的,但其对认知障碍PDPN的具体贡献尚不清楚.
研究的目的:
- 在患有PDPN和认知障碍的糖尿病小鼠中调查肠道微生物群和代谢物概况.
- 探索连接肠道变化与这些并发症的潜在机制.
主要方法:
- 利用小鼠和对照,评估疼痛和认知功能.
- 通过16S rRNA测序和便代谢物使用LC-MS分析了肠道微生物组合.
- 测量了神经纤维密度,神经纤维标记物和促炎细胞因子.
主要成果:
- 与对照组相比,小鼠表现出PDPN和认知缺陷,与肠道微生物群和代谢物配置不同.
- 特定的细菌 (例如,Muribaculaceae,Ruminococcus) 和代谢物 (Dl-乳酸,多甲酸) 被确定为介质.
- 微生物群和代谢物变化与DRG和海马体中益炎性细胞因子增加相关.
结论:
- 肠道微生物群和代谢物与糖尿病小鼠的PDPN和认知功能障碍密切相关.
- 这些发现表明涉及Dl-乳酸和多甲酸的潜在机制.
- 调节肠道微生物群和代谢物可能为糖尿病并发症提供新的治疗策略.
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