AJCN EB Program 2010
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lieber, C. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lieber, C. S.
Agricola
Right arrow Articles by Lieber, C. S.

American Journal of Clinical Nutrition, Vol 58, 430-442, Copyright © 1993 by The American Society for Clinical Nutrition, Inc

REVIEW ARTICLES

Herman Award Lecture, 1993: a personal perspective on alcohol, nutrition, and the liver

CS Lieber
Section of Liver Disease and Nutrition, Bronx Veterans' Affairs Medical Center, New York 10468.

Alcohol causes primary malnutrition by displacing nutrients in the diet and secondary malnutrition via malabsorption and cellular injury through direct cytotoxicity. Hepatotoxicity results from metabolic disturbances associated with the oxidation of ethanol via liver alcohol dehydrogenase (ADH) and the redox changes produced by the generated NADH (the reduced form of nicotinamide adenine dinucleotide), which in turn affects the metabolism of lipids, carbohydrates, proteins, and purines. Ethanol is also oxidized in liver microsomes by an ethanol- inducible cytochrome P450, which contributes to the alcoholic's tolerance and his increased vulnerability to the toxicity of industrial solvents, anesthetics, commonly prescribed drugs, over-the-counter analgesics, chemical carcinogens, and retinoids. Increased acetaldehyde generation, with formation of protein adducts, results in antibody production, enzyme inactivation, decreased DNA repair, impaired utilization of oxygen, glutathione depletion, free radical-mediated toxicity, lipid peroxidation, and increased collagen synthesis. Therapy may eventually improve with the use of supernutrients such as S- adenosyl-L-methionine, which replenishes glutathione, restores methylation, and attenuates liver injury, as well as dilinoleoylphosphatidylcholine, which prevents cirrhosis.


This article has been cited by other articles:


Home page
 Exp. Biol. Med.Home page
P. R. V. Kashireddy and M. S. Rao
Sex Differences in Choline-Deficient Diet-Induced Steatohepatitis in Mice
Experimental Biology and Medicine, February 1, 2004; 229(2): 158 - 162.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Epidemiol. Biomarkers Prev.Home page
L. A. Poirier, C. K. Wise, R. R. Delongchamp, and R. Sinha
Blood Determinations of S-Adenosylmethionine, S-Adenosylhomocysteine, and Homocysteine: Correlations with Diet
Cancer Epidemiol. Biomarkers Prev., June 1, 2001; 10(6): 649 - 655.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Clin. Nutr.Home page
J. H Weisburger
Approaches for chronic disease prevention based on current understanding of underlying mechanisms
Am. J. Clinical Nutrition, June 1, 2000; 71(6): 1710S - 1714.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Clin. Nutr.Home page
M. A Leo and C. S Lieber
Alcohol, vitamin A, and {beta}-carotene: adverse interactions, including hepatotoxicity and carcinogenicity
Am. J. Clinical Nutrition, June 1, 1999; 69(6): 1071 - 1085.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1993 by The American Society for Nutrition