Overview
A decade or so ago the concept of vitamin D metabolism was deceptively simple. The vitamin was produced in the skin (vitamin D3, cholecalciferol) under the influence of the ultraviolet component of sunlight or was derived from some food sources (largely vitamin D2, ergocalciferol). These vitamins D were equally potent in man so the term vitamin D was commonly used. This vitamin, bound to a serum vitamin D binding protein (DBP), was transferred in the blood to the liver, where it was converted to 25-hydroxy- vitamin D (see Fig. 1). This metabolite also bound to the DBP was carried in blood to the kidney, which was the sole site of a further 1a-hydroxylation to produce the active hormonal form, 1, 25-dihydroxyvitamin D. The form of this hormone derived from vitamin D3 has been given the trivial name of calcitriol. However, clinically this was sometimes used to imply both 1, 25-dihydroxycholecalciferol and 1, 25-dihydroxyergocalciferol. The 24- hydroxylation pathway, which also existed in the kidney, was seen as an alternate to 1-hydroxylation and of uncertain significance. The hormone was considered to act like other steroidal hormones through a receptor but it had not been cloned and its structure was unknown. Despite this gap it was “clear” that the receptor existed in the vitamin D target organs, primarily bone and gut, and presumably not elsewhere.
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References
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Eisman, J.A. (1993). Vitamin D Metabolism. In: Physiology and Pharmacology of Bone. Handbook of Experimental Pharmacology, vol 107. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77991-6_10
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