Vitamin D3 is well-known as a major regulator of calcium and phosphorus homeostasis. A growing body of evidence highlights its crucial role in the regulation of reproductive processes in females. The role of vitamin D3 in the female reproductive tract has been extensively investigated because its receptor is abundant in reproductive organs, including ovary. Importantly, besides expression of vitamin D3 receptor, the ovary is an extrarenal site of vitamin D3 metabolism. The influence of vitamin D3 on follicular development and ovarian steroidogenesis has been investigated. Furthermore, vitamin D3 deficiency has also been associated with polycystic ovary syndrome, premature ovarian failure and ovarian cancer. The objective of this review is to summarize our knowledge about the contribution of vitamin D3 to physiological and pathological processes within the ovary.

Vitamin D₃ (VD₃) plays an important role in the ovary and its deficiency is associated with ovarian pathologies, including polycystic ovary syndrome (PCOS). However, there is no data related to VD₃ metabolism in the ovary during PCOS. Herein, we investigated differences in the expression of VD₃ receptor (VDR) and key VD₃ metabolic enzymes, 1α-hydroxylase (CYP27B1) and 24-hydroxylase (CYP24A1), in the ovary and periovarian adipose tissue (POAT) of control (proestrus and diestrus) and PCOS induced by letrozole rats. Vdr, Cyp27b1 and Cyp24a1 mRNA expression was determined, their protein abundance was examined and immunolocalized. Furthermore, VD₃ metabolite concentrations in plasma (25OHD) and tissues (ovary and POAT; 1,25(OH)₂D₃), and plasma calcium level were determined. 25OHD concentration decreased markedly in letrozole-treated rats in comparison with controls, whereas calcium concentration did not vary among the examined groups. The amount of 1,25(OH)₂D₃ decreased in both ovary and POAT of PCOS rats. In the ovary, we found decreased Cyp27b1 and increased Vdr mRNA expression in letrozole-treated and diestrus control group. Corresponding protein abundances were down-regulated and up-regulated, respectively but only following letrozole treatment. In POAT, only Cyp27b1 transcript level and CYP27B1 protein abundance were decreased in letrozole-treated rats. VDR was immunolocalized in healthy and cystic follicles, while CYP27B1 and CYP24A1 were found exclusively in healthy ones. Concluding, our results provide the first evidence of disrupted VD₃ metabolism in the ovary and POAT of PCOS rats. The reduced 1,25(OH)₂D₃ concentration in those tissues suggests their contribution to VD₃ deficiency observed in PCOS and might implicate in PCOS pathogenesis.