Mineral regulation of vitamin D metabolism

This is the authors' abstract. We don't add key points for this paper.

The pediatrician's interest in vitamin D metabolism stems from the once-endemic rachitic deformities induced by vitamin D deficiency; later, clinical research of inherited forms of rickets established further principles of vitamin D metabolism and action. Constantine Anast, as both clinician and researcher, maintained an enthusiastic interest in vitamin D metabolism. His investigative esprit fostered my interest, as a fellow in his laboratory, in the synthetic pathway of active vitamin D. The best known active metabolite of vitamin D, 1,25(OH)2D, is formed by 1βhydroxylation of 25(OH)D, the most abundant circulating form of the vitamin. This well-characterized biochemical conversion is the rate-limiting reaction in the synthesis of 1,25(OH)2D [1]. The classical homeostatic role of 1,25(OH)2D is predominantly that of a calcemie agent, an action largely resulting from the metabolite's stimulation of intestinal transport of calcium [2]. Intestinal phosphorus transport, to a lesser extent than calcium transport can be stimulated by 1,25(OH)2D [3]. Furthermore, skeletal [4] and perhaps renal activity [5] of 1,25(OH)2D can increase circulating concentrations of calcium. These in vivo effects of 1,25(OH)2D on mineral homeostasis raise the question of whether feedback control, via mineral regulation of 1,25(OH)2D production, exists, and the significant mechanisms involved. Here, I will briefly review evidence from earlier studies supporting the notion of calcium and phosphorus regulation of 1α-hydroxylase activity, and present data generated in collaboration with Dr Anast examining vitamin D metabolism in magnesium deficiency.