Lu Shelly C, Martínez-Chantar M Luz, Mato José M
USC Liver Disease Research Center, USC-UCLA Alcoholic Liver and Pancreatic Disease Center, Division of Gastrointestinal and Liver Diseases, Department of Medicine, Keck School of Medicine USC, Los Angeles, California 90033, USA.
J Gastroenterol Hepatol. 2006 Oct;21 Suppl 3:S61-4. doi: 10.1111/j.1440-1746.2006.04575.x.
Methionine adenosyltransferase (MAT) is an essential enzyme that catalyzes the formation of the principal methyl donor S-adenosylmethionine (SAMe). Studies in the past decade have shown that SAMe is not only a methyl donor, but also a key metabolite that regulates hepatocyte growth, death and differentiation. Abnormalities in MAT and decreased SAMe levels occur in experimental animals and humans with alcoholic liver disease. Chronic hepatic SAMe deficiency can result in the spontaneous development of steatohepatitis and hepatocellular carcinoma. This paper reviews MAT genes and SAMe in relation to alcoholic liver disease and the molecular mechanisms by which SAMe regulates hepatocyte growth and apoptosis.
甲硫氨酸腺苷转移酶（MAT）是一种催化主要甲基供体S-腺苷甲硫氨酸（SAMe）形成的关键酶。过去十年的研究表明，SAMe不仅是一种甲基供体，还是调节肝细胞生长、死亡和分化的关键代谢物。在患有酒精性肝病的实验动物和人类中，MAT会出现异常，SAMe水平也会降低。慢性肝脏SAMe缺乏可导致脂肪性肝炎和肝细胞癌的自发发展。本文综述了与酒精性肝病相关的MAT基因和SAMe，以及SAMe调节肝细胞生长和凋亡的分子机制。
