Gascon-Barré M
Am J Physiol. 1982 May;242(5):G522-32. doi: 10.1152/ajpgi.1982.242.5.G522.
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.
在维生素D缺乏的雌性大鼠中，研究了静脉注射或十二指肠内注射完整的[3H]-25-羟基维生素D3（[3H]25(OH)D3）后以及十二指肠内再次给予[3H]25(OH)D3衍生的胆汁物质后3小时内[3H]25(OH)D3的胆汁排泄情况。每组给予四剂25(OH)D3（0.25、2.5、25和250 nmol/100 g）。在所研究的剂量范围内，[3H]25(OH)D3的胆汁排泄无法饱和，这表明在25(OH)D3中毒情况下，25(OH)D3的胆汁排泄是一种可靠的解毒机制。对血浆、肝脏和胆汁的分析表明，胆小管膜似乎是25(OH)D3胆汁排泄的限速因素。十二指肠内给予源自[3H]25(OH)D3的胆汁排泄化合物表明，它们能有效地在新分泌的胆汁中再次排泄，证实了25(OH)D3存在肠肝循环。然而，在这组动物中，血浆分析表明这些化合物进入体循环的量微不足道，这表明肠肝循环在机体25(OH)D3代谢中可能起有限作用。
