抗生素可以减轻饮食引起的非酒精性脂肪肝疾病,而不会改变肠道屏障功能障碍
Annette Brandt1, Katja Csarmann1, Angélica Hernández-Arriaga2
1Department of Nutritional Sciences, Molecular Nutritional Science, University of Vienna, Vienna, Austria.
抗生素在小鼠中预防了非酒精性脂肪肝疾病 (NAFLD) 的发展,但没有修复肠道屏障功能障碍. 果糖,而不是肠道细菌,似乎通过氧化 (NO) 途径驱动这种功能障碍.
科学领域:
- 胃肠病学 胃肠病学
- 肝病学 肝病学是一种肝病学.
- 微生物学 微生物学
背景情况:
- 非酒精性脂肪肝 (NAFLD) 与肠道屏障功能障碍有关.
- 肠道微生物群变化的特定作用在NAFLD相关的屏障功能障碍中仍然不清楚.
研究的目的:
- 研究抗生素对NAFLD发展和小鼠肠道屏障功能的影响.
- 阐明NAFLD中饮食诱导的肠壁功能障碍背后的机制.
主要方法:
- 雄性C57BL/6J小鼠被食控制或高脂肪,高果糖饮食,有或没有抗生素7周.
- 评估肝损伤,炎症,肠道透性 (西洛斯),紧结蛋白,微生物群和氧化合成酶 (NOS) 活性.
- 对果糖和NOS抑制剂暴露的隔离肠道组织囊.
主要成果:
- 在高果糖饮食小鼠中,抗生素消除了肝硬化和炎症.
- 尽管接受了抗生素治疗,肠道屏障缺陷 (透性,iNOS) 仍然存在.
- 果糖在体外增加了肠道透性和紧结蛋白损失,这种效应不是通过抗生素调解的,而是通过NOS抑制减弱的.
结论:
- 在饮食引起的NAFLD中,肠壁功能障碍可能不是主要源于微生物群的变化.
- 肠道氧化物 (NO) 恒温的果糖诱导的改变似乎对NAFLD的屏障功能障碍至关重要.
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