Augustyn Monika, Grys Iwon, Kukla Michał
Department of Internal Medicine and Gastroenterology, 5 Military Hospital with Polyclinic in Cracow, Poland.
Department of Gastroenterology and Hepatology, Medical University of Silesia in Katowice, Poland.
Clin Exp Hepatol. 2019 Mar;5(1):1-10. doi: 10.5114/ceh.2019.83151. Epub 2019 Feb 20.
The gut microbiota has recently been recognized as a major environmental factor in the pathophysiology of several human diseases. The anatomical and functional association existing between the gut and the liver provides the theoretical basis to assume that the liver is a major target for gut microbes. In the last decades, many studies have reported an altered composition of gut microbiota in patients with chronic liver diseases and liver cirrhosis, suggesting a progressively marked dysbiosis to be related to worsening of the liver disease. Modifications of microbiota result in alteration in providing signals through the intestine and bacterial products, as well as hormones produced in the bowel that affect metabolism at different levels including the liver. There is increasing evidence for a correlation between intestinal microbiota, bacterial translocation and hepatic steatosis. Intestinal microbiota affects nutrient absorption and energy homeostasis. Altered intestinal permeability may favor the passage of bacteria derived compounds into the systemic circulation, causing a systemic inflammatory state, characteristic of the metabolic syndrome. At present, an increasing number of studies indicate a close relationship between dysbiosis, defined as abnormal composition and the amount of intestinal bacteria (gut microbiota), intestinal permeability and some metabolic, inflammatory, degenerative and even psychiatric diseases. Microbiota pharmacological modulation seems to be a promising tool for a new therapeutic approach to non-alcoholic fatty liver disease and in prevention of cirrhosis. The following study aims to briefly discuss the role of microbiota disorder (dysbiosis), and in particular small intestinal bacterial overgrowth (SIBO), in the pathogenesis of nonalcoholic fatty liver disease (NAFLD).
肠道微生物群最近被认为是几种人类疾病病理生理学中的一个主要环境因素。肠道与肝脏之间存在的解剖学和功能联系为假定肝脏是肠道微生物的主要靶器官提供了理论基础。在过去几十年中，许多研究报告了慢性肝病和肝硬化患者肠道微生物群的组成发生了改变，这表明日益明显的生态失调与肝病的恶化有关。微生物群的改变会导致通过肠道和细菌产物以及肠道产生的影响包括肝脏在内的不同水平代谢的激素提供信号发生改变。越来越多的证据表明肠道微生物群、细菌易位与肝脂肪变性之间存在关联。肠道微生物群影响营养吸收和能量稳态。肠道通透性改变可能有利于细菌衍生化合物进入体循环，导致全身炎症状态，这是代谢综合征的特征。目前，越来越多的研究表明生态失调（定义为肠道细菌的组成和数量异常，即肠道微生物群）、肠道通透性与一些代谢性、炎症性、退行性甚至精神性疾病之间存在密切关系。微生物群的药物调节似乎是一种有前途的工具，可用于非酒精性脂肪性肝病的新治疗方法和预防肝硬化。以下研究旨在简要讨论微生物群紊乱（生态失调），特别是小肠细菌过度生长（SIBO）在非酒精性脂肪性肝病（NAFLD）发病机制中的作用。
