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Intestinally derived bacterial products stimulate development of nonalcoholic steatohepatitis. | LitMetric

Intestinally derived bacterial products stimulate development of nonalcoholic steatohepatitis.

Pharmacol Res

NuMeCan Institute (Nutrition, Metabolism and Cancer), Université de Rennes, INSERM, INRA, F-35000 Rennes, France. Electronic address:

Published: March 2019

AI Article Synopsis

Article Abstract

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.

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Source
http://dx.doi.org/10.1016/j.phrs.2019.01.026DOI Listing

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