Evidence for the Promotion of Bone Mineralization by 1α,25-Dihydroxycholecalciferol in the Rat Unrelated to the Correction of Deficiencies in Serum Calcium and Phosphorus

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Abstract
Concurrent administration of 1α,25-dihydroxycholecalciferol [1α,25-(OH)2-CC] to intact and thyroparathyroidectomized rats treated with ethane-1-hydroxy-1,1-diphosphonate (EHDP) prevented or reversed the EHDP-induced inhibition of bone mineralization as measured by changes in epiphyseal plate width and ash content of bone. An analog, 1α-hydroxycholecalciferol, was also effective. Recovery of bone after EHDP treatment was also significantly improved by administration of 1α,25-(OH)2-CC as evidenced by enhanced uptake of 45Ca by epiphyseal plates and decreased plate widths. Cholecalciferol (CC), ergocalciferol, dihydrotachysterol2, 5,6-trans-CC, 25-OH-CC, 5,6-trans-25-OH-CC, and 1α,24R,25-(OH)3-CC also blocked EHDP-induced epiphyseal plate widening, but required high, pharmacological dose levels. 24R,25-(OH)2-CC was inactive at doses up to 10 µg/day. Since EHDP-treated rats are not deficient in calcium or phosphate, these data suggest that 1α,25-dihydroxycholecalciferol promoted bone mineralization independently of effects upon the intestinal absorption of calcium and phosphate.