Knodell R G, Kinsey M, Boedeker E C, Collin D P
Gastroenterology. 1976 Aug;71(2):196-201.
Deoxycholate is often absent in bile of patients with alcoholic cirrhosis. The purpose of this study was to define the mechanism for this abnormality in bile acid metabolism in alcoholic cirrhosis. Excretion and hepatic metabolism of exogenous [14C]deoxycholate were determined, quantitative and qualitative analyses of fecal bile acids were performed, and ability of fecal bacteria to metabolize cholate to deoxycholate in vitro was measured both in cirrhotic patients and in controls. There was no evidence for deoxycholate malabsorption or rehydroxylation. In cirrhotic patients without biliary deoxycholate, both in vivo levels of deoxycholate and lithocholate in feces and in vitro fecal bacterial conversion of cholate to deoxycholate were significantly decreased as compared to controls. The marked decrease in 7 alpha-dehydroxylase activity of fecal bacteria of some patients with alcoholic cirrhosis results in impaired conversion of cholate to deoxycholate and explains the lack of biliary deoxycholate in these patients.
酒精性肝硬化患者的胆汁中通常缺乏脱氧胆酸。本研究的目的是确定酒精性肝硬化患者胆汁酸代谢异常的机制。测定了外源性[14C]脱氧胆酸的排泄和肝脏代谢,对粪便胆汁酸进行了定量和定性分析,并测量了肝硬化患者和对照组粪便细菌在体外将胆酸代谢为脱氧胆酸的能力。没有证据表明存在脱氧胆酸吸收不良或再羟化。在没有胆汁脱氧胆酸的肝硬化患者中,与对照组相比,粪便中脱氧胆酸和石胆酸的体内水平以及粪便细菌在体外将胆酸转化为脱氧胆酸的能力均显著降低。一些酒精性肝硬化患者粪便细菌的7α-脱羟基酶活性显著降低,导致胆酸转化为脱氧胆酸受损,这解释了这些患者胆汁中缺乏脱氧胆酸的原因。