<原著>無菌マウスにおける実験的胆石形成と肝コレステロール代謝系酵素

概要

論文の詳細を見る
As to the cause of cholesterol gallstone, lithogenesis based on bite acids, cholesterol and lecithin relates closely with the changes in liver cholesterol metabolic enzyme activity. Therefore, germ-free mice and conventional mice were given an experimental diet containing 0.5% cholesterol and 0.25% cholic acid, and the lithogenesis rate, activities of the enzymes and so on were determined for each animal group (n : 10), over time. Gallstones were formed in 50% of the conventional mice 8 weeks after going on the experimental diet and in 80% after 12 weeks. In 100% of the germ-free mice, gallstones were formed 8 weeks after going on the diet. Plasma and liver lipid levels increased slightly in the conventional mice and markedly in the germ-free mice, their lipid level increasing to about five times higher than that of the control level. Of the liver cholesterol metabolic enzymes, the ratio of acyl CoA : cholesterol acyltransferase/neutral cholesterol esterase tended to rise, which accelerated the accumulation of cholesterol ester in the liver. The activity of cholesterol 7α-hydroxylase was depressed in the germ-free mice, while it was enhanced at the 8th week in the conventional mice given the experimental diet. This result was attributable to the activation of bite acid biosynthesis as the compensatory mechanism for cholesterol loading. Further the cholic acid group/chenode-oxycholic acid group (CA/CDCA) ratio of the bite acid composition at this period was increased in mice receiving the experimental diet, in comparison with mice receiving an ordinary diet, the increase being particularly marked in the germ-free mice. Since increase in the CA/CDCA ratio is thought to enhance the reabsorption of cholesterol and bite acid in the intestine, bile may be more liable to be lithogenous in germ-free mice than in conventional mice. Cholesterol loading causes an increase in the intracorporeal cholesterol pool and a depressing tendency in the activity of liver cholesterol 7α-hydroxylase, or the rate-limiting enzyme of bile acid biosynthesis. The catabolism of liver cholesterol to bile acid is depressed and bile supersaturated with cholesterol is formed. Consequently, cholesterol precipitates as crystals, causing lithogenesis. Thus, it is reasonable to presume as follows : because the above-mentioned tendency appeared earlier and more markedly in germ-free mice (without catabolic activity of cholesterol in the intestine) than in conventional mice, gallstones were formed more frequently in the former than in the latter.
近畿大学の論文
1986-03-25

<原著>無菌マウスにおける実験的胆石形成と肝コレステロール代謝系酵素

スポンサーリンク

概要

著者

関連論文

スポンサーリンク