Fig. 1

The involvement of gut microbiota and their resulting substances in the progression of NAFLD. The products generated by gut microorganisms, encompassing monosaccharides, short-chain fatty acids (SCFAs), bile acids (BAs), and trimethylamine oxide (TMAO), assume crucial roles not only in the liver’s energy metabolism and the cellular lining of the intestines but also exert a direct influence on the production of liver fat and overall systemic inflammation. A range of molecular elements come into play, including adenosine monophosphate-dependent protein kinase (AMPK), carbohydrate-responsive element-binding protein (ChREBP), Cytochrome P450 7A1 (CYP7A1), farnesoid X receptor (FXR), glucagon-like peptide-1 (GLP-1), G protein-coupled receptor 41/43 (GPCR41/43), peptide YY (PYY), sterol regulatory element-binding protein 1 (SREBP-1), and Takeda G protein receptor 5 (TGR5). Collectively, these elements contribute to these effects