Importance of a deficiency in S-adenosyl-L-methionine synthesis in the pathogenesis of liver injury

被引：67

作者：

Martínez-Chantar, ML ^{[1
]}

García-Trevijano, ER ^{[1
]}

Latasa, MU ^{[1
]}

Pérez-Mato, I ^{[1
]}

del Pino, MMS ^{[1
]}

Corrales, FJ ^{[1
]}

Avila, MA ^{[1
]}

Mato, JM ^{[1
]}

机构：

[1] Univ Navarra, Sch Med, Div Hepatol & Gene Therapy, Pamplona 31008, Spain

来源：

AMERICAN JOURNAL OF CLINICAL NUTRITION | 2002年 / 76卷 / 05期

关键词：

methionine; S-adenosyl-L-methionine; SAMe; methionine adenosyltransferase; liver injury; liver regeneration; cirrhosis; oxidative stress; protein S-nitrosylation;

D O I：

10.1093/ajcn/76.5.1177S

中图分类号：

R15 [营养卫生、食品卫生]; TS201 [基础科学];

学科分类号：

100403 ;

摘要：

One of the features of liver cirrhosis is an abnormal metabolism of methionine-a characteristic that was described more than a half a century ago. Thus, after an oral load of methionine, the rate of clearance of this amino acid from the blood is markedly impaired in cirrhotic patients compared with that in control subjects. Almost 15 y ago we observed that the failure to metabolize methionine in cirrhosis was due to an abnormally low activity of the enzyme methionine adenosyltransferase (EC 2.5.1.6). This enzyme converts methionine, in the presence of ATP, to S-adenosyl-L-methionine (SAMe), the main biological methyl donor. Since then, it has been suspected that a deficiency in hepatic SAMe may contribute to the pathogenesis of the liver in cirrhosis. The studies reviewed here are consistent with this hypothesis.

引用

页码：1177S / 1182S

页数：6

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