Martínez-Chantar M Luz, García-Trevijano Elena R, Latasa M Ujue, Pérez-Mato Isabel, Sánchez del Pino Manuel M, Corrales Fernando J, Avila Matias A, Mato José M
Division of Hepatology and Gene Therapy, School of Medicine, University of Navarra, Pamplona, Spain.
Am J Clin Nutr. 2002 Nov;76(5):1177S-82S. doi: 10.1093/ajcn/76/5.1177S.
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.
肝硬化的特征之一是蛋氨酸代谢异常——这一特征在半个多世纪前就有描述。因此，口服蛋氨酸负荷后，与对照受试者相比，肝硬化患者血液中这种氨基酸的清除率明显受损。大约15年前，我们观察到肝硬化患者蛋氨酸代谢失败是由于蛋氨酸腺苷转移酶（EC 2.5.1.6）的活性异常低下。该酶在ATP存在的情况下将蛋氨酸转化为S-腺苷-L-蛋氨酸（SAMe），即主要的生物甲基供体。从那时起，人们就怀疑肝脏SAMe缺乏可能有助于肝硬化肝脏的发病机制。这里综述的研究与这一假设一致。
