Gut-liver axis, nutrition, and non-alcoholic fatty liver disease.
Gut-liver axis, nutrition, and non-alcoholic fatty liver disease.
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DOI：
10.1016/j.clinbiochem.2015.06.023
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发表时间：
2015-09
影响因子：
2.8
通讯作者：
McClain CJ
中科院分区：
文献类型：
--
作者：
Kirpich IA;Marsano LS;McClain CJ
非酒精性脂肪性肝病（NAFLD）代表了一系列涉及肝脏脂肪蓄积、炎症以及随时间推移可能进展为纤维化和肝硬化的疾病。NAFLD通常与肥胖、胰岛素抵抗和糖尿病有关。肝脏和肠道之间的相互作用，即所谓的“肠-肝轴”，在NAFLD的发病和进展中起着关键作用。令人信服的证据将肠道微生物组，肠道屏障完整性和NAFLD联系起来。饮食因素可能改变肠道微生物群和肠道屏障功能，有利于代谢性内毒素血症和低度炎症的发生，从而促进肥胖和肥胖相关脂肪肝疾病的发展。用益生元和益生菌调节肠道微生物群并维持肠道屏障完整性的治疗操作是NAFLD管理的潜在药剂。本文综述了目前关于NAFLD发病机制中肠道微生物群、肠道屏障和饮食因素之间复杂相互作用的知识。本综述中所涉及的概念具有重要的临床意义，尽管需要做更多的工作来了解饮食因素如何影响肠道屏障和微生物群，并了解微生物衍生成分如何干扰宿主的代谢，从而促进NAFLD的发展。
Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of diseases involving hepatic fat accumulation, inflammation with the potential progression to fibrosis and cirrhosis over time. NAFLD is often associated with obesity, insulin resistance, and diabetes. The interactions between the liver and the gut, the so-called ”gut-liver axis”, play a critical role in NAFLD onset and progression. Compelling evidence links the gut microbiome, intestinal barrier integrity, and NAFLD. The dietary factors may alter the gut microbiota and intestinal barrier function, favoring the occurrence of metabolic endotoxemia and low grade inflammation, thereby contributing to the development of obesity and obesity-associated fatty liver disease. Therapeutic manipulations with prebiotics and probiotics to modulate the gut microbiota and maintain intestinal barrier integrity are potential agents for NAFLD management. This review summarizes the current knowledge regarding the complex interplay between the gut microbiota, intestinal barrier, and dietary factors in NAFLD pathogenesis. The concepts addressed in this review have important clinical implications, although more work needs to be done to understand how dietary factors affect the gut barrier and microbiota, and to comprehend how microbe-derived components may interfere with the host’s metabolism contributing to NAFLD development.