Kolb E
Z Gesamte Inn Med. 1976 Aug 1;31(15):561-7.
A survey is given on the present state of the animal-biochemical research concerning the effectivity of the D-vitamins. The vitamin D3 is transferred in 25-hydroxycholecalciferol in the microsome fraction of the liver. Then in the kidneys a transformation into the physiologically active forms - the 1,25- and the 24,25-hydroxycholecalciferol - takes place. The kind of transformation depends on the Ca- and P-supply as well as on the level of the parathormone secretion. In the mucous membrane of the small intestine the 1,25- and the 24,25-hydroxycholecalciferol stimulate the formation of the Ca-transport protein. The 1,25-hydroxycholecalciferol is above all formed in hypocalcaemia or hypophosphataemia and furthers the mobilisation of Ca- and phosphate-ions from the bones. In a liver damage disturbances of the formation of 25-hydroxycholecalciferol and in renal damage disturbances of the formation of 1,25- and 24,25-hydroxycholecalciferol may appear. A reduction of the formation of the active forms of the D-vitamins leads to a decrease of the Ca-utilisation as well as of the growth of bones.
本文综述了关于维生素D有效性的动物生化研究现状。维生素D3在肝脏微粒体部分转化为25-羟胆钙化醇。然后在肾脏中转化为生理活性形式——1,25-二羟胆钙化醇和24,25-二羟胆钙化醇。转化的类型取决于钙和磷的供应以及甲状旁腺激素的分泌水平。在小肠黏膜中，1,25-二羟胆钙化醇和24,25-二羟胆钙化醇刺激钙转运蛋白的形成。1,25-二羟胆钙化醇主要在低钙血症或低磷血症时形成，并促进钙和磷酸根离子从骨骼中的动员。在肝脏损伤时，可能会出现25-羟胆钙化醇形成障碍；在肾脏损伤时，可能会出现1,25-二羟胆钙化醇和24,25-二羟胆钙化醇形成障碍。维生素D活性形式的形成减少会导致钙利用率降低以及骨骼生长减缓。
