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胆盐缺乏与维生素D代谢产物的吸收。大鼠体内研究。

Bile salt deficiency and the absorption of vitamin D metabolites. In vivo study in the rat.

作者信息

Maislos M, Shany S

机构信息

Department of Medicine C, Toor Institute, Soroka Medical Center, Beer Sheva, Israel.

出版信息

Isr J Med Sci. 1987 Nov;23(11):1114-7.

PMID:2830204
Abstract

We studied the effect of the absence of bile salts on the absorption of vitamin D metabolites in vivo, in the biliary duct-ligated rat. The mesenteric, lymphatic absorption of the metabolites studied (vitamin D3, 25-hydroxyvitamin D3, and 1,25-dihydroxyvitamin D3) was almost completely abolished in the experimental animals. These results differed significantly (P less than 0.001) from those of the control rats. The 1,25-dihydroxyvitamin D3 absorption into the portal vein system was unaffected by the lack of biliary salts. The absorption of 25-hydroxyvitamin D3 was decreased and that of vitamin D3 was negligible, under the same experimental conditions. These data show that the more polar vitamin D metabolites, like 1,25-dihydroxyvitamin D3 and to some extent 25-hydroxyvitamin D3, are absorbed directly into the portal blood without the involvement of bile salts and micelle formation. Thus, the use of polar vitamin D metabolites should be considered in correcting hypovitaminosis D and osteomalacia in cases of chronic biliary salt depletion.

摘要

我们在胆管结扎的大鼠体内研究了缺乏胆盐对维生素D代谢产物吸收的影响。在所研究的代谢产物(维生素D3、25-羟基维生素D3和1,25-二羟基维生素D3)的肠系膜淋巴吸收在实验动物中几乎完全被消除。这些结果与对照大鼠的结果有显著差异(P小于0.001)。缺乏胆盐并不影响1,25-二羟基维生素D3进入门静脉系统的吸收。在相同实验条件下,25-羟基维生素D3的吸收减少,而维生素D3的吸收可忽略不计。这些数据表明,极性更强的维生素D代谢产物,如1,25-二羟基维生素D3以及在一定程度上的25-羟基维生素D3,可直接吸收进入门静脉血,而无需胆盐和微胶粒形成的参与。因此,在慢性胆盐缺乏导致维生素D缺乏症和骨软化症的情况下,应考虑使用极性维生素D代谢产物来进行纠正。

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