The stimulation of 25-hydroxyvitamin D 3-1α-hydroxylase by estrogen

Abstract

Homogenates of kidney from laying Japanese quail incubated in vitro with 25-hydroxy-[26,27- 3H] vitamin D 3 produce more 1,25-dihydroxy-[26,27- 3H]vitamin D 3 than do homogenates of kidney from mature nonlaying females or males maintained on the same diet and under identical conditions. Instead, the homogenates from male quail or nonlaying female quail convert 25-hydroxyvitamin D 3 to 24,25-dihydroxyvitamin D 3. The administration of 5 mg of estradiol to mature male quail 24 h prior to sacrifice suppressed the 25-hydroxyvitamin D 3-24-hydroxylase and markedly stimulated 25-hydroxyvitamin D 3-1-hydroxylase. The administration of estradiol to male quail caused hypercalcemia, which responded more slowly than did the 1-hydroxylase. As little as 0.1 mg of estradiol/quail was found effective in stimulating the 1-hydroxylase and suppressing the 24-hydroxylase. Other hormones such as follicle stimulating hormone (FSH), cortisone, testosterone, and progesterone, even at high dose levels, produced little or no change in the 25-hydroxyvitamin D 3-1-hydroxylase. Testosterone did, however, suppress the 25-hydroxyvitamin D 3-24-hydroxylase. The stimulation of the 25-hydroxyvitamin D 3-1-hydroxylase by parathyroid hormone was of a smaller magnitude than that of the estradiol, and the effects of the two hormones were additive, suggesting that they function by a different mechanism.