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. 2015 Sep 29;6(3):55–58. doi: 10.1002/cld.494

Figure 1.

Figure 1

The gut microbiota and NAFLD. The gut bacteria may contribute to NAFLD via multiple mechanisms and pathways: 1) production of bacteria‐derived toxins, eg, LPS, which may activate TLR‐4‐ and TLR‐9‐mediated proinflammatory cytokine production in the liver macrophages resulting in hepatocellular inflammation; 2) regulation of energy homeostasis involving increased fermentation of carbohydrates to SCFAs, selective suppression of Fiaf, a circulating lipoprotein lipase inhibitor, facilitating de novo hepatic lipogenesis and deposition of triglycerides in adipocytes and the liver; 3) modulation of choline metabolism (which is required for very low‐density lipoprotein synthesis and hepatic lipid export); 4) modulation of bile acid homeostasis; and/or 5) generation of endogenous EtOH, which is known to play an important role in the disruption of intestinal TJs, causing hepatic oxidative stress and inducing liver inflammation. Abbreviations: ChREBP, carbohydrate‐responsive element‐binding protein; Fiaf, fasting‐induced adipocyte factor; EtOH, ethanol; LPL, lipoprotein lipase; NAFLD, nonalcoholic fatty liver disease; SCFAs, short chain fatty acids; SREBP‐1c, sterol regulatory element‐binding transcription factor 1; TJs, tight junctions; TLR‐4, Toll‐like receptor‐4; VLDL, very low‐density lipoprotein.