Fig. 2

Gut dysbiosis disrupts the integrity of the intestinal barrier, enabling the passage of bacterial endotoxins into the liver. This, in turn, amplifies the inflammatory processes and the accumulation of fat, contributing to the development of NAFLD. Unhealthy lifestyle choices, such as a high-fat, low-fiber diet, alter the composition of the gut microbiota. This alteration increases the permeability of the gut, leading to the production of various proinflammatory molecules, including LPS, TMAO, SBAs, and bacterial 16sDNA. These proinflammatory molecules further exacerbate liver inflammation and fibrosis, potentially accelerating the progression of NAFLD. Various interventions, such as treatment with FXR/TGR5 agonists, and probiotics play a crucial role in strengthening the tight junctions within the intestinal barrier. They also regulate glucose and lipid metabolism by activating FXR and TGR5 signaling pathways, while simultaneously inhibiting the TLR4/NF-kB and JAK1/STAT6 pathways