Abstract
Aim: We aimed to examine the alterations of the insulin signaling pathway, autophagy, nitrative stress and the effect of vitamin D supplementation in the liver and ovaries of vitamin D deficient hyperandrogenic rats. Methods: Female Wistar rats received eight weeks of transdermal testosterone treatment and lived on a low vitamin D diet (D–T+). Vitamin D supplementation was achieved by oral administration of vitamin D3 (D+T+). Sham-treated (D+T–) and vitamin D deficient animals (D–T–) served as controls. (N = 10–12 per group). Results: D–T+ animals showed decreased LC3 II levels in the liver and increased p-Akt/Akt and p-eNOS/eNOS ratios with decreased insulin receptor staining in the ovaries. Vitamin D supplementation prevented the increase of Akt phosphorylation in the ovaries. Vitamin D deficiency itself also led to decreased LC3 II levels in the liver and decreased insulin receptor staining in the ovaries. D–T+ group showed no increase in nitrotyrosine staining; however, the ovaries of D–T– rats and the liver of D+T+ animals showed increased staining intensity. Conclusion: Vitamin D deficiency itself might lead to disrupted ovarian maturation and autophagy malfunction in the liver. Preventing Akt phosphorylation may contribute to the beneficial effect of vitamin D treatment on ovarian function in hyperandrogenism.
Highlights
Polycystic ovary syndrome (PCOS) is a complex endocrine disease of fertile women, its estimated occurrence is between 5–15%
We aimed to examine the effect of vitamin D supplementation on insulin receptor signaling, autophagosomal turnover and nitrative stress in the liver and the ovaries in a vitamin D deficient hyperandrogenic rat model of PCOS
Testosterone treatment led to an elevated number of smaller, mostly primordial follicles that is typical for PCOS, and reduced serum progesterone levels caused by missing luteinisation
Summary
Polycystic ovary syndrome (PCOS) is a complex endocrine disease of fertile women, its estimated occurrence is between 5–15%. PCOS involves hyperandrogenism and ovulatory dysfunction leading to infertility or an increased rate of miscarriage. It is associated with a variety of other comorbidities including obesity, type 2 diabetes mellitus (T2DM), and non-alcoholic fatty liver disease (NAFLD) [1]. Vitamin D deficiency is shown to commonly be associated with PCOS [2,3]. Both vitamin D deficiency [4] and hyperandrogenism may contribute to the development of insulin resistance (IR) observed in women with PCOS, the underlying mechanism of IR seems to be different [5].
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