高脂肪饮食调节胆汁酸成分和肠道微生物群,影响严重胆管炎和小鼠初级胆管胆管炎的肝硬化变化
Masahiro Umemura1, Akira Honda2, Maho Yamashita1
1Department of Internal Medicine II, Hamamatsu University School of Medicine, 1-20-1 Handayama, Chuo-ku, Hamamatsu, Shizuoka, 431-3192, Japan.
Journal of autoimmunity
|July 21, 2024
概括
高脂肪饮食会通过改变胆汁酸和肠道细菌,使小鼠的初级胆汁胆道炎 (PBC) 恶化,导致肝硬化. 这突出了饮食的重点.
科学领域:
- 免疫学 免疫学 免疫学
- 胃肠病学 胃肠病学
- 微生物学 微生物学
背景情况:
- 胆汁酸 (BAs) 影响初级胆汁胆道炎 (PBC) 进展超出免疫耐受性损失.
- 饮食对PBC免疫病理学,BA组成和肠道微生物群的影响尚未完全理解.
研究的目的:
- 在一个独特的小鼠模型中,研究高脂肪饮食 (HFD) 对PBC免疫病理学和BA变化的影响.
- 在PBC的背景下分析HFD对肠道微生物群组成的影响.
主要方法:
- 使用了一个Cyp2c70/Cyp2a12双淘汰 (DKO) 鼠标模型,具有类似人类的BA组成.
- 给药2-octynoic 酸 (2OA) 诱导胆管炎,然后比较HFD与正常饮食 (ND) 在十周内的影响.
- 分析了肝细胞因子/化学因子表达,纤维化标志物,血清BA水平,BA合成基因表达和肠道微生物群组成.
主要成果:
- 在2OA治疗的DKO小鼠中,HFD显著加剧了胆管炎,导致肝硬化.
- HFD增加了肝脏Th1反应和纤维化标志物.
- HFD改变了BA配置文件,增加了石灰酸 (LCA) 和CDCA衍生的BA,同时降低了关键BA合成基因的调节.
- HFD改变了肠道微生物群,增加了乙化因子和乳球菌,并减少了Desulfovibrio和Lachnospiraceae_NK4A136_group.
结论:
- 在小鼠中,HFD通过调节BA组成和肠道微生物群来加剧PBC向肝硬化进展.
- 饮食引起的BA代谢和肠道微生物组的变化是PBC病变发生的关键因素.
- 结果提供了对人类PBC进展和潜在的饮食干预措施的见解.
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