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. Author manuscript; available in PMC: 2021 Jan 22.
Published in final edited form as: Hepatoma Res. 2021 Jan 13;7:11. doi: 10.20517/2394-5079.2020.134

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