In the present study, the role of
vitamin D in the regulation of
estrogen synthesis in gonads was investigated.
Vitamin D receptor null mutant mice showed gonadal insufficiencies. Uterine hypoplasia and impaired folliculogenesis were observed in the female, and decreased sperm count and decreased motility with histological abnormality of the testis were observed in the male. The
aromatase activities in these mice were low in the ovary, testis, and epididymis at 24%, 58%, and 35% of the wild-type values, respectively. The gene expression of
aromatase was also reduced in these organs. Elevated serum levels of LH and FSH revealed
hypergonadotropic hypogonadism in these mice. The gene expressions of
estrogen receptor alpha and beta were normal in gonads in these mice. Supplementation of
estradiol normalized histological abnormality in the male gonads as well as in the female.
Calcium supplementation increased
aromatase activity and partially corrected the
hypogonadism. When the serum
calcium concentration was kept in the normal range by supplementation, the
aromatase activity in the ovary increased to 60% of the wild-type level, but LH and FSH levels were still elevated. These results indicated that
vitamin D is essential for full gonadal function in both sexes. The action of
vitamin D on
estrogen biosynthesis was partially explained by maintaining
calcium homeostasis; however, direct regulation of the expression of the
aromatase gene should not be neglected.