Buchanan J R, Santen R, Cauffman S, Cavaliere A, Greer R B, Demers L M
Calcif Tissue Int. 1986 Sep;39(3):139-44. doi: 10.1007/BF02555109.
To test the hypothesis that estrogen modulates the metabolism of 25-hydroxyvitamin D (25(OH)D) to 1,25-dihydroxyvitamin D (1,25(OH)2D) and 24,25-dihydroxyvitamin D (24,25(OH)2D), we studied 20 normal premenopausal women at four consecutive weekly intervals during one menstrual cycle. Estrogen stimulation was semiquantitatively defined into baseline, low-grade, or medium-grade categories, based on endogenous estrone and estradiol concentrations. 1,25(OH)2D increased incrementally from baseline levels of 34 +/- 3(SE) pg/ml to 39 +/- 3 pg/ml (P = 0.2) with low-grade estrogen stimulation and to 43 +/- 3 pg/ml (P less than 0.05) with medium-grade estrogen stimulation, while 25(OH)D, 24,25(OH)2D, vitamin D binding protein, parathyroid hormone, calcium, and phosphate did not change. 24,25(OH)2D was correlated to 25(OH)D at baseline (r = 0.65, P less than 0.01) and with low-grade estrogen stimulation (r = 0.62, P less than 0.01), but not with medium-grade stimulation (r = 0.13); these relationships are consistent with the concepts that 25(OH)D is metabolized predominantly to 24,25(OH)2D at low estrogen levels, but not at higher estrogen levels. We conclude that endogenous estrogen elevation promotes formation of 1,25(OH)2D from 25(OH)D, and that it may reciprocally inhibit synthesis of 24,25(OH)2D.
为了验证雌激素调节25-羟基维生素D（25(OH)D）代谢为1,25-二羟基维生素D（1,25(OH)2D）和24,25-二羟基维生素D（24,25(OH)2D）这一假设，我们在一个月经周期内连续四周对20名正常绝经前女性进行了研究。根据内源性雌酮和雌二醇浓度，将雌激素刺激半定量地分为基线、低级别或中级别类别。随着低级别雌激素刺激，1,25(OH)2D从基线水平的34±3（标准误）pg/ml逐渐增加至39±3 pg/ml（P = 0.2），随着中级别雌激素刺激增加至43±3 pg/ml（P<0.05），而25(OH)D、24,25(OH)2D、维生素D结合蛋白、甲状旁腺激素、钙和磷均未改变。24,25(OH)2D在基线时与25(OH)D相关（r = 0.65，P<0.01），在低级别雌激素刺激时也相关（r = 0.62，P<0.01），但在中级别刺激时不相关（r = 0.13）；这些关系与以下概念一致，即25(OH)D在低雌激素水平时主要代谢为24,25(OH)2D，但在较高雌激素水平时并非如此。我们得出结论，内源性雌激素升高促进25(OH)D形成1,25(OH)2D，并且可能反过来抑制24,25(OH)2D的合成。
