Abstract
Abstract Liver homogenates hydroxylate dihydrotachysterol3 in position 25 equally well whether they are prepared from rats low in vitamin D or from rats treated with vitamin D3. This contrasts with the liver homogenate 25-hydroxylation of vitamin D3 which is markedly reduced by pretreatment with vitamin D3. In addition, the rate of appearance of 25-hydroxy[3H]dihydrotachysterol3 in the blood following a dose of [3H]dihydrotachysterol3 is not reduced by prior treatment with unlabeled vitamin D3 or dihydrotachysterol in contrast to the effect of prior vitamin D3 treatment on in vivo vitamin D3 25-hydroxylation. Furthermore the rate of appearance of 25-hydroxyvitamin D3 in the blood increases only about 2-fold with a 100-fold increase in vitamin D3 dose, while the rate of appearance of 25-hydroxydihydrotachysterol3 increases 100-fold with a 100-fold increase in dihydrotachysterol3 dose. These results strongly suggest that the 25-hydroxylation of dihydrotachysterol is not regulated in vivo as is the 25-hydroxylation of vitamin D3. They also support the idea that the regulation of calciferol-25-hydroxylase activity functions to maintain a low circulating level of 25-hydroxyvitamin D3 in the blood even when large amounts of vitamin D3 are being ingested.
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