Barak A J, Beckenhauer H C, Badakhsh S, Tuma D J
Veterans Affairs Alcohol Research Center, Department of Veterans Affairs Medical Center, Omaha, Nebraska 68105, USA.
Alcohol Clin Exp Res. 1997 Sep;21(6):1100-2.
The feeding of ethanol to experimental animals results in fatty infiltration of the liver. Recent findings have shown that ethanol-induced steatosis is accompanied by a lowering in hepatic S-adenosylmethionine (SAM) levels. It is known that SAM provides substrates for reduced glutathione formation and offers the cell protection from toxic metabolic oxidants. A recent study in this laboratory demonstrated that dietary supplementation with betaine generated increased SAM in the liver and protected against ethanol-induced steatosis. The present study not only showed that betaine supplementation to rats protects the liver from alcoholic steatosis, but also demonstrated that once steatosis is established, treatment with betaine partially reversed the steatosis after cessation of ethanol feeding. Furthermore, this study indicated that betaine supplementation to the diet had the capacity to attenuate steatosis despite the continued feeding of ethanol.
给实验动物喂食乙醇会导致肝脏脂肪浸润。最近的研究结果表明，乙醇诱导的脂肪变性伴随着肝脏S-腺苷甲硫氨酸（SAM）水平的降低。已知SAM为还原型谷胱甘肽的形成提供底物，并为细胞提供免受有毒代谢性氧化剂侵害的保护。本实验室最近的一项研究表明，饮食中补充甜菜碱可使肝脏中SAM增加，并预防乙醇诱导的脂肪变性。本研究不仅表明给大鼠补充甜菜碱可保护肝脏免受酒精性脂肪变性的影响，还证明一旦脂肪变性形成，在停止喂食乙醇后用甜菜碱治疗可部分逆转脂肪变性。此外，该研究表明，尽管持续喂食乙醇，但饮食中补充甜菜碱仍有减轻脂肪变性的能力。
