| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1995: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1994: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Research Abstract |
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.
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