Altered insulin-induced relaxation of aortic rings in a dihydrotestosterone-induced rodent model of polycystic ovary syndrome

Masszi, G. and Buday, A. and Novak, A. and Horváth, Eszter Mária and Tarszabo, R. and Sara, L. and Revesz, C. and Benko, Rita and Nádasy, György László and Benyó, Zoltán and Hamar, Péter and Várbíró, Szabolcs (2013) Altered insulin-induced relaxation of aortic rings in a dihydrotestosterone-induced rodent model of polycystic ovary syndrome. Fertility and sterility, 99 (2). pp. 574-578. ISSN 0015-0282, ESSN: 1556-5653

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Abstract

Objective: To clarify the effects of dihydrotestosterone (DHT) – induced polycystic ovary syndrome (PCOS) on the insulin-dependent vasodilatation of the thoracic aorta and the role of vitamin D in a rat model. Design: Controlled experimental animal study. Setting: Laboratory. Animal(s): Thirty adolescent female Wistar rats. Intervention(s): The PCOS model was induced by 10 weeks of DHT treatment (83 mg/d). One-half of the DHT-treated animals also received vitamin D (120 ng/kg/wk). Main Outcome Measure(s): The aortic rings of the control, DHT, and DHT plus vitamin D –treated animals were isolated. The insulin- dependent vasodilation of the isolated aortic rings was compared in Krebs-Ringer solution and under blockade of nitric oxide (NO)synthase or cyclooxygenase. Result(s): The insulin-dependent vasorelaxation decreased in both DHT-treated groups independently from the vitamin D treatment;NO-dependent and -independent relaxations were both impaired. In response to prostanoid, vasoconstriction was increased after DHT treatment. The NO-independent relaxation was partially improved by vitamin D treatment, which was neutralized by increased prostanoid-dependent vasoconstriction. Conclusion(s): Previously, we found that vitamin D treatment prevented systemic insulin resistance; however, in this study, we did not detect any influence on the vascular insulin resistance of the aorta that was induced by DHT treatment. Consequently, controlling insulin resistance with vitamin D alone did not resolve the aortic endothelial dysfunction caused by the hyperandrogenic state.

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