Arteriolar insulin resistance in a rat model of polycystic ovary syndrome

Sara, Levente and Antal, Péter and Masszi, Gabriella and Buday, Anna and Horváth, Eszter Mária and Hamar, Péter and Monos, Emil and Nádasy, György László and Várbíró, Szabolcs (2012) Arteriolar insulin resistance in a rat model of polycystic ovary syndrome. Fertility and sterility, 97 (2). pp. 462-468. ISSN 0015-0282, ESSN: 1556-5653

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Abstract

OBJECTIVE: To investigate the vascular dysfunction caused by insulin resistance in polycystic ovary syndrome (PCOS) and the effectiveness of vitamin D in an animal model. DESIGN: Controlled experimental animal study. SETTING: Animal laboratory at a university research institute. ANIMAL(S): Thirty female Wistar rats. INTERVENTION(S): Rats were divided into groups at age 21-28 weeks. Twenty of them were subjected to dihydrotestosterone (DHT) treatment (83 μg/d); ten of them also received parallel vitamin D treatment (120 ng/100 g/wk). Oral glucose tolerance tests with insulin level measurements were performed. Gracilis arterioles were tested for their contractility as well as their nitric oxide (NO)-dependent and insulin-induced dilation using pressure arteriography. MAIN OUTCOME MEASURE(S): Several physiologic parameters, glucose metabolism, and pressure arteriography. RESULT(S): DHT treatment increased the passive diameter of resistance arterioles, lowered norepinephrine-induced contraction (30.1 ± 4.7% vs. 8.7 ± 3.6%) and reduced acetylcholine-induced (122.0 ± 2.9% vs. 48.0 ± 1.4%) and insulin-induced (at 30 mU/mL: 21.7 ± 5.3 vs. 9.8 ± 5.6%) dilation. Vitamin D treatment restored insulin relaxation and norepinephrine-induced contractility; in contrast, it failed to alter NO-dependent relaxation. CONCLUSION(S): In DHT-treated rats, in addition to metabolically proven insulin resistance, decreased insulin-induced vasorelaxation was observed and was improved by vitamin D treatment without affecting NO-dependent relaxation. The reduction in insulin-induced dilation of arterioles is an important as yet undescribed pathway of vascular damage in PCOS and might explain the clinical effectiveness of vitamin D treatment.

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