Alcohol-induced fatty liver development

Inhibition of Alcohol-Induced Fatty Liver Development.239... 

From a morphological perspective, any kind of alcohol-induced fatty liver or alcoholic hepatitis has the potential to develop into cirrhosis. The fibrous ramifications of the various portal fields make contact with one another as well as with other centrilobular fibre formations. This ultimately causes pronounced fibrosis of the liver, which leads to a cirrhotic transformation if alcohol consumption continues, (s. fig. 28.7)... 

Histologically, non-alcoholic steatohepatitis shows moderate to high-grade, mainly macrovesicular fatty degeneration of the liver cells with inflammatory infiltrates and formation of fibrosis. Cirrhosis frequently develops. Despite the morphological similarity to alcohol-induced fatty liver hepatitis, there is no (noteworthy) alcohol consumption involved in NASH. Viral or autoimmune hepatitis are not detectable either. There are no or only moderate subjective complaints. The transaminases are normal or slightly increased. NASH is mostly associated with obesity and/or type II diabetes, thus NASH is regarded as the hepatic manifestation of a metabolic syndrome. 

Although just a few drinks may result in hepatic fat accumulation, chronic consumption of alcohol greatly enhances the development of a fatty liver. Re-esterification of fatty acids into triacylglycerols by fatty acyl CoA transferases in the ER is enhanced (see Fig. 25.6). Because the transferases are microsomal enzymes, they are induced by ethanol consumption just as MEOS is induced. The result is a fatty liver (hepatic steatosis). 

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