Pathogenesis of alcoholic liver disease: Role of oxidative metabolism

Figure 2 Molecular mechanisms of alcoholic fatty liver. Alcohol consumption via multiple pathways increases the expression of SREB-1 and downregulates PPAR-α, promoting fatty acid synthesis and impairing β-oxidation, thus resulting in fatty acid accumulation. Long-term ethanol consumption promotes fatty acid accumulation through decreased autophagy, while short-term ethanol exposure promotes autophagy and degradation of lipid droplets. HIF: Hypoxia inducible factor; ROS: Reactive oxygen species.