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REVIEW ARTICLE |
1 From the Division of Metabolism and Health Effects, National Institute of Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD (VP and SZ); the Division of Gastroenterology/Hepatology, Duke University Medical Center, Durham, NC (MFA); the Department of Medicine, University of Louisville, Louisville, KY (SB and CJM); the Department of Animal Sciences, University of Wisconsin, Madison, WI (NJB); the Clinical Nutrition Research Unit, Genome and Biomedical Sciences Facility, University of California Davis, Davis, CA (CHH); the Keck School of Medicine, University of Southern California, Los Angeles, CA (NK and SCL); the VA Medical Center, Liver Study Unit R-151, Omaha, NE (KKK); and the National Center for Complementary and Alternative Medicine (QYL) and the Office of Dietary Supplements (CS), National Institutes of Health, Bethesda, MD
This report is a summary of a symposium on the role of S-adenosylmethionine (SAM), betaine, and folate in the treatment of alcoholic liver disease (ALD), which was organized by the National Institute on Alcohol Abuse and Alcoholism in collaboration with the Office of Dietary Supplements and the National Center for Complementary and Alternative Medicine of the National Institutes of Health (Bethesda, MD) and held on 3 October 2005. SAM supplementation may attenuate ALD by decreasing oxidative stress through the up-regulation of glutathione synthesis, reducing inflammation via the down-regulation of tumor necrosis factor-
and the up-regulation of interleukin-10 synthesis, increasing the ratio of SAM to S-adenosylhomocysteine (SAH), and inhibiting the apoptosis of normal hepatocytes and stimulating the apoptosis of liver cancer cells. Folate deficiency may accelerate or promote ALD by increasing hepatic homocysteine and SAH concentrations; decreasing hepatic SAM and glutathione concentrations and the SAM-SAH ratio; increasing cytochrome P4502E1 activation and lipid peroxidation; up-regulating endoplasmic reticulum stress markers, including sterol regulatory element–binding protein-1, and proapoptotic gene caspase-12; and decreasing global DNA methylation. Betaine may attenuate ALD by increasing the synthesis of SAM and, eventually, glutathione, decreasing the hepatic concentrations of homocysteine and SAH, and increasing the SAM-SAH ratio, which can trigger a cascade of events that lead to the activation of phosphatidylethanolamine methyltransferase, increased phosphatidylcholine synthesis, and formation of VLDL for the export of triacylglycerol from the liver to the circulation. Additionally, decreased concentrations of homocysteine can down-regulate endoplasmic reticulum stress, which leads to the attenuation of apoptosis and fatty acid synthesis.
Key Words: Alcohol • betaine • S-adenosylmethionine • folate • liver disease
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