Monroe P, Vlahcevic Z R, Swell L
Alcohol Clin Exp Res. 1981 Jan;5(1):92-100. doi: 10.1111/j.1530-0277.1981.tb04871.x.
Ethanol has been demonstrated to cause aberrations in lipoprotein metabolism, cholesterol synthesis, biliary secretion, and bile acid synthesis. Although there is interdependency of cholesterol and bile acid metabolism, a role of ethanol-induced lipid abnormalities in altering bile acid synthesis has not been found. The direct effects of ethanol administration on bile acid metabolism have been studied in animals and vary with the experimental design. Acutely, ethanol causes decreased bile acid secretion and synthesis, but other effects are less well defined. Chronic ethanol use in man may result in cirrhosis, a condition in which abnormalities of bile acid metabolism have been described in detail. Cholic acid synthesis and pool size are markedly depressed in advanced cirrhosis. Chenodeoxycholic acid synthesis is affected less than cholic acid synthesis, probably because 12 alpha-hydroxylase activity is markedly depressed in cirrhosis, although other steps may also be influenced such as 7 alpha-hydroxylation of cholesterol or availability of cholesterol precursor. The deoxycholic acid pool is depressed probably because of changes in fecal flora. Despite the decrease in total bile acid pool, lithogenicity of bile is not increased in cirrhotic patients because of a concomitant decline in cholesterol and phospholipid secretion. Changes in hepatic blood flow and hepatic extraction cause an increase in plasma bile acid levels which may have clinical relevance.
乙醇已被证明会导致脂蛋白代谢、胆固醇合成、胆汁分泌和胆汁酸合成异常。尽管胆固醇和胆汁酸代谢相互依存，但尚未发现乙醇诱导的脂质异常在改变胆汁酸合成中的作用。乙醇给药对胆汁酸代谢的直接影响已在动物中进行研究，且因实验设计而异。急性情况下，乙醇会导致胆汁酸分泌和合成减少，但其他影响尚不清楚。人类长期饮酒可能导致肝硬化，在这种情况下，胆汁酸代谢异常已被详细描述。在晚期肝硬化中，胆酸合成和池大小明显降低。鹅去氧胆酸合成受到的影响小于胆酸合成，这可能是因为肝硬化时12α-羟化酶活性明显降低，尽管其他步骤如胆固醇的7α-羟化或胆固醇前体的可用性也可能受到影响。脱氧胆酸池降低可能是由于粪便菌群的变化。尽管总胆汁酸池减少，但由于胆固醇和磷脂分泌同时下降，肝硬化患者胆汁的成石性并未增加。肝血流量和肝摄取的变化导致血浆胆汁酸水平升高，这可能具有临床意义。
