Rise in the hepatic concentration of dicarboxylic acids. In addition to increased TAG synthesis , evidence of decreased capacity of the liver to export TAG in VLDL particles . Increased hepatic levels of free fatty acids following alcohol intake. The only consensus is that fatty acid availability plays a significant role . Summary Alcoholic fatty liver results from interaction of ethanol and its oxidation products with hepatic lipid metabolism.
Early target is mitochondrial fatty acid oxidation.
Acetaldehyde and reaction oxygen species incriminated in the pathogenesis of the mitochondrial injury. Enhanced formation of triacylglycerols , partly secreted to the plasma and partly accumulate . Compensatory mechanism fades with progression of the liver injury .