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. Author manuscript; available in PMC: 2017 Feb 17.
Published in final edited form as: Curr Mol Pharmacol. 2017;10(3):195–206. doi: 10.2174/1874467208666150817111419

Fig. 1. Multiple possible pathways contribute to the development of alcohol-induced fatty liver.

Fig. 1

This schematic highlights four pathways through which chronic alcohol consumption has been proposed to cause hepatic steatosis. 1) Alcohol stimulates the uptake of circulating fatty acids into the liver, which are then used as a substrate for triacylglycerol synthesis. 2) Alcohol stimulates de novo lipogenesis, with the newly synthesized fatty acids acting as a substrate for triacylglycerol synthesis. 3) Alcohol inhibits mitochondrial β-oxidation of hepatic fatty acids, leading to their accumulation and availability for synthesis of triacylglycerol. 4). Alcohol inhibits VLDL secretion from the liver, limiting the liver’s ability to secrete triacylglycerol and causing it to accumulate. FA: fatty acids, TAG: triacylglycerol; CHO: carbohydrate; VLDL: very low-density lipoprotein.