饮食中的胆缺乏症通过微生物代谢重新连接来增强Helicobacter pylori驱动的肠肝功能障碍
Jiongle Li1, Lixin Wang1, Zixin Meng1
1Guizhou Key Laboratory of Microbio and Infectious Disease Prevention & Control, Key Laboratory of Microbiology and Parasitology of Education Department of Guizhou, School of Basic Medical Science, Guizhou Medical University, Guiyang 550025, PR China.
胆缺乏会通过改变肠道微生物和新陈代谢,使Helicobacter pylori (H. pylori) 的胃损伤恶化. 保持足够的胆摄入量对于感染H. pylori的人来说至关重要,以防止严重的健康问题.
科学领域:
- 微生物学 微生物学
- 营养科学 营养科学
- 胃肠病学 胃肠病学
背景情况:
- 杆菌 (H. pylori) 感染影响全球一半的人口,但疾病的严重程度差异很大.
- 主体的饮食和营养状况,特别是胆缺乏,与H. pylori的病原发生有关.
- 连接胆缺乏症和H. pylori引起的损伤的机制尚不清楚.
研究的目的:
- 研究胆缺乏和H. pylori感染对宿主新陈代谢和肠道微生物群的协同作用.
- 阐明胆代谢在与H. pylori相关的胃肠道和肝脏病理学中的作用.
主要方法:
- 给小鼠吃了缺乏胆的饮食 (CDD),并感染了H. pylori8至16周.
- 评估葡萄糖-脂质代谢,炎症,组织损伤和胃肠道屏障蛋白.
- 利用代谢学和16S rRNA测序来分析胆代谢和微生物变化.
主要成果:
- 杆菌感染改变了微生物胆代谢,增加了三甲基胺 (TMA) 和减少了三甲基胺N氧化物 (TMAO) 产量.
- CDD使肠道微生物易于受到H. pylori诱导的破坏,其联合效应放大了炎症和组织损伤.
- CDD和H. pylori之间的协同相互作用导致了显著的肠肝轴功能障碍.
结论:
- 胆缺乏会加剧由H. pylori诱导的肠道微生物群失调和代谢功能障碍.
- 这种恶化导致炎症和损伤的增加,特别是影响肠肝轴.
- 建议在感染H. pylori的个体中保持足够的食胆,以减轻病理后果.
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