Inhibition of vitamin D-stimulated active transport of calcium of rat intestine by diphenylhydantoin-phenobarbital treatment.
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Biomedical subjects
Publications and source records attributed to H C Harrison.
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Since the introduction of irradiated ergosterol into our food supply, nutritional vitamin D-deficiency rickets has become an uncommon disease. However, skeletal disorders due to abnormalities of vitamin D function still occur. These disorders can now be classified more exactly into two groups: those in which there is a deficiency of the active metabolite of vitamin D, 1,25-dihydroxyvitamin D, and those in which there is an abnormality of renal tubular function resulting in renal hypophosphatemia despite normal vitamin D metabolism. The various entities of these two groups are described and the theoretical basis of their treatment given.
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The activity of dihydrotachysterol and cholecalciferol was determined in nephrectomized or sham-operated vitamin D-depleted rats using in vitro transport of calcium and phosphate by everted intestinal preparations as the index of physiologic response. The activity of dihydrotachysterol was not reduced by absence of the kidneys whereas that of cholecalciferol was markedly inhibited so that at least a 10-fold greater dose of the latter was necessary to produce an equivalent effect in the nephrectomized rat as in the control. Dihydrotachysterol is therefore equipotent with cholecalciferol in the anephric rat although much less active in the intact animal.
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