Journal of Lipid Research, Vol 20, 289-315, Copyright © 1979 by Lipid Research, Inc.

REVIEWS

Effects of ethanol on lipid metabolism

E Baraona and CS Lieber

Alcohol promotes accumulation of fat in the liver mainly by substitution of ethanol for fatty acids as the major hepatic fuel. The degree of lipid accumulation depends on the supply of dietary fat. Progressive alteration of the mitochondria, which occurs during chronic alcohol consumption, decreases fatty acid oxidation by interfering with citric acid cycle activity. This block is partially compensated for by increased ketone body production, which results in ketonemia. Thus, mitochondrial damage perpetuates fatty acid accumulation even in the absence of ethanol oxidation. Alcohol facilitates esterification of the accumulated fatty acids to triglycerides, phospholipids, and cholesterol esters, all of which accumulate in the liver. The accumulated lipids are disposed of in part as serum lipoprotein, resulting in moderate hyperlipemia. In some individuals with pre- existing alterations of lipid metabolism, small ethanol dose may provoke marked hyperlipemia which responds to alcohol withdrawal. Inhibition of the catabolism of cholesterol to bile salt may contribute to the hepatic accumulation and hypercholesterolemia. The capacity of lipoprotein production and hyperlipemia development increases during chronic alcohol consumption, probably as a result of the concomitant hypertrophy of the endoplasmic reticulum and Golgi apparatus. However, this compensation is relatively inefficient in ridding the liver of fat. This inefficiency may be linked to alterations of hepatic microtubules induced by ethanol or its metabolites, which interfere with the export of protein from liver to serum, promoting hepatic accumulation of proteins as well as fat. As liver injury aggravates, hyperlipemia wanes and liver steatosis is exaggerated. Derangements of serum lipids similar to those found in other types of liver disease also become apparent. The changes in serum lipids may be a sensitive indicator of the progression of liver damage in the alcoholic.
CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				L. Kang, X. Chen, B. M. Sebastian, B. T. Pratt, I. R. Bederman, J. C. Alexander, S. F. Previs, and L. E. Nagy Chronic Ethanol and Triglyceride Turnover in White Adipose Tissue in Rats: INHIBITION OF THE ANTI-LIPOLYTIC ACTION OF INSULIN AFTER CHRONIC ETHANOL CONTRIBUTES TO INCREASED TRIGLYCERIDE DEGRADATION J. Biol. Chem., September 28, 2007; 282(39): 28465 - 28473. [Abstract] [Full Text] [PDF]

				L. Kang and L. E. Nagy Chronic Ethanol Feeding Suppresses {beta}-Adrenergic Receptor-Stimulated Lipolysis in Adipocytes Isolated from Epididymal Fat Endocrinology, September 1, 2006; 147(9): 4330 - 4338. [Abstract] [Full Text] [PDF]

				M. BEDNARSKA-MAKARUK, M. RODO, C. MARKUSZEWSKI, A. ROZENFELD, M. SWIDERSKA, B. HABRAT, and H. WEHR POLYMORPHISMS OF APOLIPOPROTEIN E AND ANGIOTENSIN-CONVERTING ENZYME GENES AND CAROTID ATHEROSCLEROSIS IN HEAVY DRINKERS Alcohol Alcohol., July 1, 2005; 40(4): 274 - 282. [Abstract] [Full Text] [PDF]

				Y. Hashimoto, T. Nakayama, A. Futamura, M. Omura, H. Nakarai, and K. Nakahara Relationship between Genetic Polymorphisms of Alcohol-metabolizing Enzymes and Changes in Risk Factors for Coronary Heart Disease Associated with Alcohol Consumption Clin. Chem., July 1, 2002; 48(7): 1043 - 1048. [Abstract] [Full Text] [PDF]