Download calcium plus vitamin d1/22/2024 In a recent report, an infant with hypophosphatasia suffered vitamin D deficiency-induced rickets, although serum calcium and phosphate were always entirely normal. By promoting optimal extra-cellular calcium and phosphate concentrations, the vitamin D system ensures the mineralization of newly deposited bone and cartilage matrix. In systemic VDR knock-out model, rickets and osteomalacia can be prevented by a diet rich in calcium and phosphate with lactose supplements to improve intestinal calcium absorption. Infusion of calcium and phosphate in vitamin D-deficient rats results in normal mineralization of hypertrophic cartilage and bone. Vitamin D status is evaluated by the measurement of circulating 25-hydroxyvitamin D (25OHD), preferentially with a standardized assay. Vitamin D deficiency impairs hypertrophic cartilage and bone mineralization, leading to rickets in children and osteomalacia in adults. Calcitriol is a potent stimulator of bone resorption, by increasing the expression and production of RANKL by osteoblasts. Calcitriol stimulates intestinal trans-epithelial transport of calcium and phosphate through both genomic and non-genomic mechanisms. The latter step is stimulated by PTH, IGF-I and by low calcium or phosphate intakes or concentrations. Synthesized in the skin under the influence of UV light, vitamin D (cholecalciferol) undergoes a first hydroxylation in position 25 in the liver, leading to 25-hydroxyvitamin D (calcifediol), and a second one in position 1 in the kidney, leading to the active metabolite 1,25-dihydroxyvitamin D (calcitriol). Vitamin D is an important regulator of calcium and phosphate homeostasis.
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