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Figure 1: Potential mechanisms underlying the alcoholic fatty liver. In liver, sterol regulatory element binding protein 1 is responsible for fatty acid synthesis and peroxisome proliferator activated receptor-α, AMPdependent protein kinase (AMPK) and adiponectin are responsible for fatty acid oxidation. Ethanol may influence the activity of PPAR-α, SREBP-1, and AMPK directly or through adiponectin and tumor necrosis factor-α. These effects activate the lipogenic pathways and inhibit fatty acid oxidation. Besides the fatty acid synthesis and oxidation, ethanol also alters lipid droplets (LD, the storage form of TG) metabolism in hepatocytes and very low-density lipoproteins secretion from liver. All these alterations contribute to alcohol-induced fatty liver

Figure 1: Potential mechanisms underlying the alcoholic fatty liver. In liver, sterol regulatory element binding protein 1 is responsible for fatty acid synthesis and peroxisome proliferator activated receptor-α, AMPdependent protein kinase (AMPK) and adiponectin are responsible for fatty acid oxidation. Ethanol may influence the activity of PPAR-α, SREBP-1, and AMPK directly or through adiponectin and tumor necrosis factor-α. These effects activate the lipogenic pathways and inhibit fatty acid oxidation. Besides the fatty acid synthesis and oxidation, ethanol also alters lipid droplets (LD, the storage form of TG) metabolism in hepatocytes and very low-density lipoproteins secretion from liver. All these alterations contribute to alcohol-induced fatty liver