Microbial metabolites in non-alcoholic fatty liver disease - PubMed (original) (raw)

Review

Microbial metabolites in non-alcoholic fatty liver disease

Da Zhou et al. World J Gastroenterol. 2019.

Abstract

The prevalence of non-alcoholic fatty liver disease (NAFLD) is rising exponentially worldwide. The spectrum of NAFLD includes non-alcoholic fatty liver, non-alcoholic steatohepatitis, liver cirrhosis, and even hepatocellular carcinoma. Evidence shows that microbial metabolites play pivotal roles in the onset and progression of NAFLD. In this review, we discuss how microbe-derived metabolites, such as short-chain fatty acids, endogenous ethanol, bile acids and so forth, contribute to the pathogenesis of NAFLD.

Keywords: Microbial metabolites; Non-alcoholic steatohepatitis; Short-chain fatty acids.

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Conflict of interest statement

Conflict-of-interest statement: No potential conflicts of interest.

Figures

Figure 1

Figure 1

Effects of microbial metabolites on non-alcoholic fatty liver disease via the gut-liver axis. SCFAs: Short-chain fatty acids; I3A: Indole-3-acetic acid; IPA: Indole propionic acid; GPR41/43: G-protein-coupled receptors 41/43; ZO-1: Zonula occludens 1; GLP-1: Glucagon-like peptide-1; PYY: Peptide YY; TLR4: Toll-like receptor 4; FMO3: Flavin-containing monooxygenase 3; TMAO: Trimethylamine-N-oxide; FXR: Farnesoid X receptor; TGR5: Takeda G-protein-coupled receptor 5; S1PR2: Sphingosine 1-phosphate receptor 2; BCAAs: Branched-chain amino acids.

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