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. 2021 Jan 13:7:11.
doi: 10.20517/2394-5079.2020.134. eCollection 2021.

Gut microbiota and their metabolites in the progression of non-alcoholic fatty liver disease

Affiliations

Gut microbiota and their metabolites in the progression of non-alcoholic fatty liver disease

Jin Zhou et al. Hepatoma Res. .

Abstract

Non-alcoholic fatty liver disease (NAFLD) is the most prevalent liver disorder worldwide. It comprises a spectrum of conditions that range from steatosis to non-alcoholic steatohepatitis, with progression to cirrhosis and hepatocellular carcinoma. Currently, there is no FDA-approved pharmacological treatment for NAFLD. The pathogenesis of NAFLD involves genetic and environmental/host factors, including those that cause changes in intestinal microbiota and their metabolites. In this review, we discuss recent findings on the relationship(s) of microbiota signature with severity of NAFLD and the role(s) microbial metabolites in NAFLD progression. We discuss how metabolites may affect NAFLD progression and their potential to serve as biomarkers for NAFLD diagnosis or therapeutic targets for disease management.

Keywords: Non-alcoholic fatty liver disease; gut microbiome; gut microbiota metabolites.

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Conflict of interest statement

Conflicts of interest All authors declared that there are no conflicts of interest.

Figures

Figure 1
Figure 1
Gut microbial homeostatic balance is maintained under normal conditions. Gut microbiota produced SCFAs, namely acetate, butyrate, and propionate, influence hepatic metabolism by changing epigenetics/gene expression or directly via energy metabolism. Liver produced bile acids (such as cholic acids) are also processed by gut microbiota and released systemically. There is substantial microbial dysbiosis during NAFLD that causes SIBO of Gram-negative bacteria while reducing the overall microbial diversity. This bacterial overgrowth leads to produce proinflammatory molecules such as LPS, ethanol, TMAO, and bacterial 16sDNA. These proinflammatory molecules worsen the liver inflammation and fibrosis and potentially accelerate NAFLD progression. SCFAs: short chain fatty acids; SIBO: small intestinal bacterial overgrowth; LPS: Lipopolysaccharides; TMAO: trimethylamine N-oxide; NAFLD: Non-alcoholic fatty liver disease

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