Alterations of biliary lipid composition in patients with fatty liver and those with cholesterol gallstone disease

胆固醇过饱和胆汁的形成是胆固醇结石疾病的先决条件。为了阐明胆固醇结石患者胆固醇过饱和胆汁形成的机制，除了肝脏的胆固醇生成和胆汁酸的合成外，我们还重点研究了胆囊壁和小肠的运动，这两种运动在维持胆汁酸的肠-肝循环中起重要作用。与正常对照组相比，胆石症患者胆汁酸的小肠转运和吸收无明显延长和损害。因此，患者可能不会表现出胆汁酸循环池减少的特征，因此他们的胆汁不会因胆固醇而变得过饱和。然而，在胆囊排空障碍的患者中，胆汁酸的小肠转运和吸收明显延长和受损。在这种情况下，胆汁过饱和可能是由于胆汁酸分布的变化导致循环胆汁酸池减少所致，例如，胆汁酸滞留到低动力胆囊部和肠部。与对照组相比，胆石症患者肝脏新生胆固醇合成显著减少。进一步认为，在胆固醇过饱和胆汁的形成过程中，外源性胆固醇的高分泌可能起着重要作用。

Formation of cholesterol supersaturated bile is a prerequisite for cholesterol gallstone disease. In order to elucidate mechanisms responsible for cholesterol supersaturated bile formation in patients with cholesterol gallstone disease, we focused on the motility of the gallbladder and small intestine, both of which are important in maintaining enterohepatic circulation of bile acids, in addition to the hepatic cholesterogenesis and bile acid synthesis. In gallstone patients with intact gallbladder emptying, the small intestinal transit and absorption of bile acids were not prolonged and impaired, as compared with control subjects. Therfore, the patients may not exhibit the characteristics of a decrease in circulating pool of bile acids, and accordingly their gallbladder bile does not become supersaturated with cholesterol. However, in patients with impaired gallbladder emptying, the small intestinal transit and absorption of bile acids were significantly prolonged and impaired. In such cases, the supersaturation of gallbladder bile may be due to the reduced pool of circulating bile acids brought about by changes in bile acid distribution, e.g., a sequestration into the hypomotile gallbladder and intestine. In gallstone patients, hepatic de novo cholesterol synthesis was significantly decreased as compared with control subjects. it is further suggested that in the formation of cholesterol supersaturated bile a hypersecretion of cholesterol derived from an exogeneous source may play a significant role.