Biliary excretion of [3H]-25-hydroxyvitamin D3 in the vitamin D-depleted rat.
The biliary excretion of [3H]-25-hydroxyvitamin D3 ([3H]25(OH)D3) was studied in vitamin D-depleted female rats over a 3-h period after intravenous or intraduodenal administration of intact [3H]25(OH)D3 and after the intraduodenal readministration of the [3H]25(OH)D3-derived biliary material. In each group four doses of 25(OH)D3 were administered (0.25, 2.5, 25, and 250 nmol/100 g). Over the dose range studied, the biliary excretion of [3H]25(OH)D3 could not be saturated, indicating that the biliary excretion of 25(OH)D3 is a reliable detoxification mechanism in circumstances of 25(OH)D3 intoxication. Analysis of plasma, liver, and bile suggests that the canalicular membrane seems to be rate limiting in the biliary excretion of 25(OH)D3. The intraduodenal administration of biliary excretion compounds derived from [3H]25(OH)D3 showed that they are efficiently reexcreted in newly secreted bile, confirming the existence of an enterohepatic circulation for 25(OH)D3. In this group of animals, however, the plasma analysis indicates that these compounds reach the systemic circulation in insignificant quantities, suggesting that the enterohepatic circulation probably plays a limited role in the body 25(OH)D3 economy.
D000818:Animals; D002112:Calcifediol; D004305:Dose-Response Relationship, Drug; D004764:Enterohepatic Circulation; D005260:Female; D006500:Hepatic Duct, Common / Q000378:metabolism*; D006887:Hydroxycholecalciferols / Q000008:administration & dosage / Q000378:metabolism* / Q000627:therapeutic use; D051381:Rats; D011919:Rats, Inbred Strains; D014316:Tritium; D014808:Vitamin D Deficiency / Q000188:drug therapy / Q000378:metabolism*
D006887:Hydroxycholecalciferols; D014316:Tritium; D002112:Calcifediol