NuMeCan Institute (Nutrition, Metabolism and Cancer), Université de Rennes, INSERM, INRA, F-35000 Rennes, France.
Pharmacol Res. 2019 Mar;141:418-428. doi: 10.1016/j.phrs.2019.01.026. Epub 2019 Jan 15.
Fatty livers are susceptible to factors that cause inflammation and fibrosis, but fat deposition and the inflammatory response can be dissociated. While nonalcoholic fatty liver disease (NAFLD), caused by pathologic fat accumulation inside the liver, can remain stable for several years, in other cases NAFLD progresses to nonalcoholic steatohepatitis (NASH), which is characterized by fat accumulation and inflammation and is not a benign condition. In this review, we discuss the NASH host cells and microbial mechanisms that stimulate inflammation and predispose the liver to hepatocyte injury and fibrotic stages via increased lipid deposition. We highlight the interactions between intestine-derived bacterial products, such as lipopolysaccharide, and nutritional models of NAFLD and/or obese individuals. The results of modulating enteric microbiota suggest that gut-derived endotoxins may be essential determinants of fibrotic progression and regression in NASH.
脂肪肝易受引起炎症和纤维化的因素影响，但脂肪沉积和炎症反应可以分离。虽然由肝脏内病理性脂肪堆积引起的非酒精性脂肪肝 (NAFLD) 可以稳定数年，但在其他情况下，NAFLD 会进展为非酒精性脂肪性肝炎 (NASH)，其特征是脂肪堆积和炎症，并非良性疾病。在这篇综述中，我们讨论了 NASH 的宿主细胞和微生物机制，这些机制通过增加脂质沉积来刺激炎症，并使肝脏易受肝细胞损伤和纤维化阶段的影响。我们强调了肠源性细菌产物（如脂多糖）与 NAFLD 和/或肥胖个体的营养模型之间的相互作用。调节肠道微生物组的结果表明，肠道来源的内毒素可能是非酒精性脂肪性肝炎纤维化进展和消退的重要决定因素。
