Department of Internal Medicine, Genome and Biomedical Research Facility, University of California, Davis, CA, USA.
Adv Nutr. 2011 Sep;2(5):421-7. doi: 10.3945/an.111.000661. Epub 2011 Sep 6.
Emerging evidence indicates that ethanol-induced alterations in hepatic methionine metabolism play a central role in the pathogenesis of alcoholic liver disease (ALD). Because malnutrition is a universal clinical finding in this disease and hepatic methionine metabolism is dependent upon dietary folate and vitamins B-6 and B-12, ALD can be considered an induced nutritional disorder that is conditioned by alcohol abuse. The present review describes the etiologies of these 3 vitamin deficiencies in ALD and how they interact with chronic ethanol exposure to alter hepatic methionine metabolism. Subsequent sections focus on molecular mechanisms for the interactions of aberrant methionine metabolism with ethanol in the pathogenesis of ALD, in particular the role of S-adenosylmethionine (SAM) in regulating the epigenetic expressions of genes relevant to pathways of liver injury. The review will conclude with descriptions of studies on the efficacy of SAM in the treatment of ALD and with discussion of potentially fruitful future avenues of research.
新出现的证据表明,乙醇引起的肝蛋氨酸代谢改变在酒精性肝病(ALD)的发病机制中起核心作用。由于营养不良是这种疾病的普遍临床发现,而肝蛋氨酸代谢依赖于饮食叶酸以及维生素 B-6 和 B-12,因此可以认为 ALD 是一种由酒精滥用引起的诱导性营养障碍。本综述描述了 ALD 中这 3 种维生素缺乏的病因,以及它们如何与慢性乙醇暴露相互作用,改变肝蛋氨酸代谢。随后的部分重点介绍了异常蛋氨酸代谢与乙醇在 ALD 发病机制中的相互作用的分子机制,特别是 S-腺苷甲硫氨酸(SAM)在调节与肝损伤途径相关基因的表观遗传表达中的作用。综述将描述 SAM 治疗 ALD 的疗效研究,并讨论未来有希望的研究方向。