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. 2023 Jun 26;119(9):1787–1798. doi: 10.1093/cvr/cvad095

Figure 1.

Figure 1

The pathogenesis of non-alcoholic fatty liver disease (NAFLD) is multifactorial. Diet and dietary components effect intestinal microbiota and influence hepatic inflammation and steatosis. FFAs, reactive oxygen species (ROS), and low-grade inflammation mediate insulin resistance by altering IKK-β. Increased lipogenesis and free cholesterol further add cellular stress (lipotoxicity). LPS activates hepatic Kupffer cells to produce pro-inflammatory cytokines. SCFAs and TMAO are metabolites derived from diet components through the intestinal microbiota. Together, different mechanisms induce inflammation (e.g. production of pro-inflammatory cytokines), which activates stellate cells to produce collagen and induce fibrogenesis. FFA, free fatty acids; FXR, Farnesoid X receptor; IKK-β, inhibitor of nuclear factor kappa-B kinase subunit beta; IL-1b, interleukin 1 beta; LPS, lipopolysaccharide; MST-3 and MST-4, GCKIII kinases Mammalian sterile 20-like 3 and 4; NF-κB, nuclear factor of activated B cells; ROS, reactive oxygen species; SCFA, Short chain fatty acids; TAG, triacylglycerol; TGFβ, transforming growth factor beta; TMAO, trimethylamine-N-oxide; TNF-α, tumour necrosis factor alpha.