Androgen and Estrogen Receptor Activation Impacts Cardiac Function in a PCOS-Prone Rodent Model

Abstract Introduction: The global risk and incidence of cardiovascular disease (CVD) is increased in polycystic ovary syndrome (PCOS). Early factors subclinical CVD includes atherogenic dyslipidemia, obesity, insulin resistance, blood pressure, atherosclerosis impaired cardiac function. Androgen exposure associated with onset adiposity, insulin-glucose lipid metabolism, dysfunction. mechanisms dysfunction PCOS related to hyperandrogenemia, AR estrogen receptor (ER) activation remain unclear. Aim: aim this study was investigate the effect androgen treatment on ER activation, fatty acid metabolism function a PCOS-prone rodent model. Methods: A model at 6 wks age apoB-remnant lipemia controls were treated testosterone for 12 weeks. Cardiac assessed using transthoracic doppler echocardiography (M-Mode 2D-imaging), lipogenic, AR, other metabolic gene protein expression RTPCR SDS-PAGE western blot. Results: animals exhibited left ventricular (LV) hypertrophy, LV mass body weight (551.6 ± 38.85 mg vs 999 96.17 mg, p<0.05), posterior wall diastolic diameter internal compared controls. Isovolumetric relaxation time (IVRT) prolonged (15.91 1.591 msec 23.75 0.722 msec, p<0.05). Mild systolic evidenced by isovolumetric contraction (IVCT; 22.5 1.348 28.96 1.248 p<0.05) decreased % ejection fraction fractional shortening T mass, IVCT IVRT but did not exacerbate animals. PPAR-⍺ controls, ACC tended be reduced, ER-⍺ reduced both control Conclusions: demonstrates early hypertrophy diastolic-systolic alters are altered morphology conditions.