Abstract
Efficient intestinal calcium (Ca) and phosphate (Pi) absorption is necessary for optimal bone mineralization during growth, the protection of bone in adults, and the prevention of osteoporosis. They are both regulated by vitamin D through activation of the intestinal vitamin D receptor (VDR). Ca and Pi absorption each occurs through vitamin D-regulated, saturable pathways that predominate when dietary intake is low, and through diffusion pathways that predominate when dietary intake is high. Habitual low Ca or Pi intake upregulates their saturable transport pathway through increased renal 1,25(OH)2D production while low vitamin D status limits Ca and Pi absorption by reducing the saturable pathways. Deletion of genes that mediate vitamin D action (i.e., VDR) or production (CYP27B1) severely limits basal Ca and Pi absorption and the adaptation of mice to low Ca, but not low Pi, diets. Various physiologic or disease states modify vitamin D-regulated intestinal absorption of Ca (enhanced during late pregnancy, reduced due to menopause and aging) and P (influenced by chronic kidney disease).
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