Shaw S, Lieber C S
Gastroenterology. 1978 Apr;74(4):677-82.
Plasma amino acid abnormalities are common in alcoholics, but the respective role of alcoholism, nutrition, and liver injury in producing these abnormalities is unknown. To elucidate this question, amino acids were measured in 56 alcoholics and 32 nonalcoholics with liver disease, and in an experimental model of alcoholic liver injury in the baboon. Dietary protein deficiency depressed branched-chain amino acids with a tendency to decreased alpha-amino-n-butyric acid. By contrast, chronic alcoholic consumption selectively increased these amino acids both in short term (2 to 4 weeks) studies in human beings and in 1 to 4-year studies in baboons. Moderate liver injury had no significant effects on these amino acids whereas advanced cirrhosis depressed branched-chain amino acids. Thus, plasma branched-chain amino acids and alpha-amino-n-butyric acid in the alcoholic are affected by at least three variables: dietary protein deficiency and advanced cirrhosis which tend to decrease these amino acids, and chronic alcohol consumption which tends to increase them.
血浆氨基酸异常在酗酒者中很常见,但酗酒、营养和肝损伤在导致这些异常中各自所起的作用尚不清楚。为了阐明这个问题,对56名酗酒者、32名患有肝病的非酗酒者以及狒狒酒精性肝损伤实验模型中的氨基酸进行了测量。饮食蛋白质缺乏会降低支链氨基酸,并使α-氨基-n-丁酸有减少的趋势。相比之下,在人体的短期(2至4周)研究以及狒狒的1至4年研究中,长期饮酒会选择性地增加这些氨基酸。中度肝损伤对这些氨基酸没有显著影响,而晚期肝硬化会降低支链氨基酸。因此,酗酒者血浆中的支链氨基酸和α-氨基-n-丁酸至少受三个变量影响:饮食蛋白质缺乏和晚期肝硬化倾向于降低这些氨基酸,而长期饮酒则倾向于增加它们。