Vitamin D binding proteins.
Vitamin D binding proteins.
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维生素 D 结合蛋白。
DOI:
10.1007/978-1-4613-9934-6_2
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发表时间:
1982
影响因子:
--
通讯作者:
HaddadJr,JG
中科院分区:
文献类型:
--
作者:
HaddadJr,JG
In recent years, considerable growth has occurred in our understanding of the distribution, metabolism, and action of antiricketic sterols. Vitamin D is recognized to be synthesized in the skin, absorbed from the intestine, and transformed to more potent bioactive metabolites. Whether derived from cutaneous transformation of 7-dehydrocholesterol or dietary sources, vitamin D enters the liver where it is metabolized to 25-hydroxyvitamin D (25-OHD) by microsomal (De-Luca and Schnoes, 1976) and/or mitrochondrial (Björkhem and Holmberg, 1978) hydroxylases. Subsequently, 25-OHD can be metabolized to an array of dihy-droxylated forms of vitamin D. The most potent of these sterols in calcium translocation at the intestine and skeleton is 1,25-dihydroxyvitamin D [1,25-(OH)2D], a product of kidney (Fraser and Kodicek, 1970) cell metabolism. The production of 1,25-(OH)2D is closely regulated, perhaps most strikingly by the trophic action of parathyroid hormone (Fraser and Kodicek, 1973). Other metabolites have been isolated arid identified, but their physiological significance awaits clarification (DeLuca, 1979).