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Abstract
The production of bile salts by rat liver is regulated by a feedback mechanism, but it is not known which enzyme controls endogenous bile acid synthesis. In order to demonstrate the biochemical site of this control mechanism, bile fistula rats were infused intravenously with (14)C-labeled bile acid precursors, and bile acid biosynthesis was inhibited as required by intraduodenal infusion of sodium taurocholate. The infusion of taurocholate (11-14 mg/100 g of rat per hr) inhibited the incorporation of acetate-1-(14)C, mevalonolactone-2-(14)C, and cholesterol-4-(14)C into bile acids by approximately 90%. In contrast, the incorporation of 7alpha-hydroxycholesterol-4-(14)C into bile acids was reduced by less than 10% during taurocholate infusion. These results indicate that the regulation of bile acid biosynthesis is exerted via cholesterol 7alpha-hydroxylase provided that hepatic cholesterol synthesis is adequate.
Highlights
The infusion of taurocholate (11-14 mg/100 g of rat per hr) inhibited the incorporation of acetate-IJ4C, mevalonolactoneW4C, and cholester01-4-~~iCnto bile acids by approximately 90%
These results indicate that the regulation of bile acid biosynthesis is exerted via cholesterol 7a-hydroxylase provided that hepatic cholesterol synthesis is adequate
The results of the present experiments further suggest that negative feedback control of bile acid biosynthesis from cholesterol is exerted via the enzyme which catalyzes the 7a-hydroxylation of cholesterol
Summary
The infusion of taurocholate (11-14 mg/100 g of rat per hr) inhibited the incorporation of acetate-IJ4C, mevalonolactoneW4C, and cholester01-4-~~iCnto bile acids by approximately 90%. Specific radioactivities of biliary bile acids were determined either 60 hr following surgery, or 60 hr after bile salt infusion had been discontinued. If a precursor is acted upon by a rate-limiting enzyme, its rate of incorporation into bile acid would be smaller in a rat with a n intact enterohepatic circulation than in an animal with biliary diversion.
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