Journal
ALCOHOL
Volume 34, Issue 1, Pages 45-48Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.alcohol.2004.08.004
Keywords
alcoholic steatosis; fat oxidation; fat synthesis; malonyl coenzyme A; long-chain acyl-coenzyme A; omega-3 polyunsaturated fatty acids
Categories
Ask authors/readers for more resources
The pathogenesis of alcoholic steatosis is a complex process that is manifested through several mechanisms involving some of or all the following body metabolism components: increased fat synthesis, increased mobilization of depot fat, defective export of fat from the liver, and decreased fat breakdown. Some of the novel findings in these mechanisms involve the down-regulation of peroxisome proliferator-activated receptor alpha and up-regulation of lipogenic enzymes through the induction of sterol regulatory element-binding protein. Yet another mechanism that remains viable is the adenosine 5'-monophosphate-activated protein kinase, which, through a complex mechanism, may regulate the relative concentrations of intracellular malonyl coenzyme A and long-chain acyl-coenzyme A, the key metabolites responsible for the balance between fat synthesis versus degradation pathways. Finally, excess dietary intake of omega-6 polyunsaturated fatty acids may exacerbate alcohol-induced onset of hepatic steatosis and alcoholic liver disease. This may explain why supplementation with lecithin containing omega-6 polyunsaturated fatty acids in a recent clinical trial in human beings failed to show any beneficial effects, although it was partially effective in an animal model. In contrast, dietary intake of omega-3 polyunsaturated fatty acids in moderation may have a protective effect against steatosis and alcoholic liver disease. (C) 2005 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available