P154 Effect of Vitamin D Deficiency on Insulin Induced Vasodilatation and Receptor Expression in Rat Model of Polycystic Ovary Syndrome

Abstract

In polycystic ovary syndrome (PCOS) hyperandrogenism and metabolic dysfunction increase cardiovascular risk. Vitamin D3 deficiency is a common comorbidity in PCOS. Our aim was to examine the alterations of insulin-induced vasodilation and receptor expression in rat aorta in a PCOS model. Methods: Female Wistar rats were treated as follows: 1. vitamin D supplemented group (D+T−); 2. vitamin D deficient (D−T−), 3. vitamin D supplemented with transdermal testosterone application (D+T+) and 4. vitamin D deficient with transdermal testosterone (D−T+). Wire myograph was used for testing insulin relaxation of aorta rings in physiological salt solution and under NOS inhibition. Insulin (IR) and vitamin D receptor (VDR) density was examined by immunohistochemistry. Results: Insulin-induced vasodilatation of the aorta rings were significantly lower in both vitamin deficient compared to the vitamin supplemented groups (p < 0.05). NOS inhibition significantly reduce the relaxation. Aorta endothelial IR expression was significantly higher in the vitamin D deficient group, meanwhile in the testosterone-treated groups (D+T+; D−T+) the expression was significantly lower (Area%: D+: 0.830 ± 0.10; D+T+: 0.298 ± 0.06; D−: 1.364 ± 0.12; D−T+: 0.354 ± 0.15, p < 0.05 in D− & D+T+ & D−T+ vs D+. p < 0.01 D+T+ & D−T+ vs D−). VDR density was significantly higher in the vitamin D deficient groups in comparison to the supplemented groups (Area% VDR: D+: 41.56 ± 5.58 vs D−: 60.63 ± 5.23) Testosterone treatment have not any effect on VDR expression. Conclusion: Vitamin-D deficiency causes impaired insulin induced vasodilation. Increased IR density could not compensate altered insulin-induced relaxation.