微生物群入侵和肠-脂肪-肝轴在与代谢功能障碍相关的脂肪性肝病中
Daria Igudesman1, Gongxin Yu1, Charlene Dauriat2
1AdventHealth Translational Research Institute, Orlando, Florida, USA.
概括
微生物群侵入并不能直接表明代谢功能障碍相关的脂肪性肝病 (MASLD) 的严重程度. 然而,肠道基因表达将微生物群变化与胰岛素抵抗和MASLD联系起来.
科学领域:
- 胃肠病学和肝病学
- 微生物学 微生物学
- 代谢疾病 代谢疾病
背景情况:
- 与代谢功能障碍相关的脂肪性肝病 (MASLD) 影响了近一半的成年人,原因尚不清楚.
- 肠道微生物群与MASLD有关,但人类研究面临微生物变异性挑战.
- 这项研究调查了肠道表型,包括微生物群侵占,作为MASLD的潜在病理特征.
研究的目的:
- 确定微生物群侵占和相关的肠道表型是否是MASLD的病理特征.
- 探索肠道表型,肠道透性,结肠组织病理学和MASLD中的胰岛素抵抗之间的关系.
- 调查结肠基因表达,微生物入和与MASLD相关的代谢终点之间的相关性.
主要方法:
- 从MASLD患者和对照组收集了西格结肠活检.
- 使用粘液免疫染色和光 in situ 杂交的量化微生物群入侵.
- 评估了肠道透性,结肠组织病理学和胰岛素耐药性;进行了RNA测序和加权基因网络相关性分析.
主要成果:
- 在MASLD患者和对照人群中,微生物入并没有显著差异.
- 肠道透性和结肠组织病理学在各组中都相似.
- 微生物群侵入与调节胰岛素和脂质代谢的结肠基因网络相关,与脂肪组织的胰岛素抵抗 (Adipo-IR) 和肝硬化/纤维化途径有关.
结论:
- 微生物群侵占和相关的肠道表型与MASLD的严重程度没有相关性.
- 在胰岛素信号传递和脂质代谢中结肠基因表达将微生物入与阿迪波-IR和MASLD联系起来.
- 需要进一步的研究,以了解结肠基因产品与基于微生物群的MASLD机制的相互作用.
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