Hepatic triacylglycerol accumulation

Cunnane SC. 1987. Hepatic triacylglycerol accumulation induced by ethanol and carbon tetrachloride interactions with essential fatty acids and prostaglandins. Alcoholism Clin Exp Res 11 25-31. 

Cha, J.Y., Mameda, Y Yamamoto, K., Oogami, K. and Yanagita, T. (1998) Association Between Hepatic Triacylglycerol Accumulation Induced by Administering Orotic Acid and Enhanced Phosphatidate Phosphohydrolase Activity in Rats, Biosci. Biotechnol. Biochem. 62,508-513. 

The observations made in PPARa -/- mice (Lee et al., 1995) provide in vivo evidence for a major role of PPARa in regulating these enzymes. In PPARa -/-mice, Aoyama et al. (Aoyama et al., 1998) observed a marked decrease in the expression of genes involved in fatty acid-catabolizing enzymes. Consistent with an impaired ability to degrade fatty acid, PPARa-/- mice accumulate hepatic triacylglycerols (Costet et al., 1998). 

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). 

Other rare lipid-storage diseases include Wolman s disease (triacylglycerol and cholesterol accumulation), hepatic cholesterol ester storage disease, ceroid storage disease, histiocytosis X, lipid proteinosis, lipid dermatoarthritis and Farber s disease (see Table 12.5 involves storage of acid mucopoly-... 

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