S-adenosylmethionine (SAMe) therapy in liver disease: A review of current evidence and clinical utility

被引:170
作者
Anstee, Quentin M. [1 ]
Day, Christopher P. [1 ]
机构
[1] Newcastle Univ, Sch Med, Inst Cellular Med, Liver Res Grp, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England
关键词
S-adenosyl-L-methionine; SAMe; Hepatitis; Steatohepatitis; Oxidative stress; ADENOSYL-L-METHIONINE; CULTURED RAT HEPATOCYTES; INTRAHEPATIC CHOLESTASIS; FATTY LIVER; NONALCOHOLIC STEATOHEPATITIS; URSODEOXYCHOLIC ACID; HEPATIC METHIONINE; OXIDATIVE STRESS; ADENOSYLTRANSFERASE GENES; PHOSPHOLIPID METHYLATION;
D O I
10.1016/j.jhep.2012.04.041
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
S-adenosyl-L-methionine (SAMe; Ado Met) is an important, metabolically pleiotropic molecule that participates in multiple cellular reactions as the precursor for the synthesis of glutathione and principle methyl donor required for methylation of nucleic acids, phospholipids, histones, biogenic amines, and proteins. SAMe synthesis is depressed in chronic liver disease and so there has been considerable interest in the utility of SAMe to ameliorate disease severity. Despite encouraging pre-clinical data confirming that SAMe depletion can exacerbate liver injury and supporting a hepatoprotective role for SAMe therapy, to date no large, high-quality randomised clinical trials have been performed that establish clinical utility in specific disease states. Here, we offer an in-depth review of the published scientific literature relating to the physiological and pathophysiological roles of SAMe and its therapeutic use in liver disease, critically assessing implications for clinical practice and offering recommendations for further research. (C) 2012 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:1097 / 1109
页数:13
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