Gascon-Barré M
Horm Metab Res. 1982 Jun;14(6):332-3.
Plasma 25-(OH)D3 concentrations following an intra-portal injection of 100 micrograms Kg-1 of D3 or 100 micrograms Kg-1 of 25-(OH)D3 was studied in D depleted rats fed ethanol diet and pair-fed controls. When challenged with D3, the rats under ethanol feeding were unable to increase their plasma 25(OH)D3 concentrations above those observed in controls. Plasma 25(OH)D3 concentrations following 25(OH)D3 administration were however lowered by the ethanol treatment 3 and 96 hr after 25(OH)D3 administration (p less than 0.05). These results suggest that animals chronically exposed to ethanol have an unaltered plasma 25(OH)D3 response following a pharmacological dose of D3 while the drug treatment contributes to an accelerated plasma 25(OH)D3 disappearance following 25(OH)D3. The former observations also suggest that D3 does not seem to be a high affinity substrate for the ethanol-induced cytochrome P-450.
在喂食乙醇饮食的维生素D缺乏大鼠及其配对喂食的对照大鼠中,研究了经门静脉注射100微克/千克的维生素D3或100微克/千克的25-(羟基)维生素D3后血浆25-(羟基)维生素D3的浓度。当用维生素D3刺激时,喂食乙醇的大鼠无法使其血浆25(羟基)维生素D3浓度升高至高于对照组所观察到的水平。然而,在给予25(羟基)维生素D3后3小时和96小时,乙醇处理降低了给予25(羟基)维生素D3后的血浆25(羟基)维生素D3浓度(p<0.05)。这些结果表明,长期暴露于乙醇的动物在给予药理剂量的维生素D3后血浆25(羟基)维生素D3反应未改变,而药物处理导致给予25(羟基)维生素D3后血浆25(羟基)维生素D3加速消失。先前的观察结果还表明,维生素D3似乎不是乙醇诱导的细胞色素P-450的高亲和力底物。