THE question whether vitamin D acts directly at sites of bone formation or indirectly at sites of calcium and phosphate absorption has long been a source of argument, with no general conclusion reached. Treatment of rachitic chicks with 1-hydroxyvitamin D3, the synthetic analogue of 1,25-dihydroxyvitamin D3, does not prevent most of the changes seen in bone affected by rickets, in spite of normal plasma levels of calcium and inorganic phosphate (unpublished). Similar findings have been reported for man1, suggesting that vitamin D affects bone formation directly and that the effect is mediated by a metabolite(s) other than 1,25-dihydroxyvitamin D3. In normocalcaemic animals, the predominant dihydroxylated metabolite of vitamin D in the blood is 24, 25-dihydroxyvitamin D and, like 1,25-dihydroxyvitamin D, it is synthesised in the kidney2,3; but nothing is known of its function. Improved calcium retention has been reported in anephric patients treated with 24,25-dihydroxyvitamin D3 (ref. 4), which has been observed to accumulate preferentially in fetal bones of rat5 and in callus tissue formed after experimental fracture (unpublished). We now report that when rachitic chicks are exposed to various therapeutic treatments with metabolites of vitamin D, the presence of 24,25-dihydroxyvitamin D is essential for the healing process.
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ORNOY, A., GOODWIN, D., NOFF, D. et al. 24, 25-Dihydroxyvitamin D is a metabolite of vitamin D essential for bone formation. Nature 276, 517–519 (1978). https://doi.org/10.1038/276517a0
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