Testosterone Treatment Impairs Cardiac Function and Fatty Acid Metabolism in a Rodent Model of Polycystic Ovary Syndrome

The incidence of cardiovascular disease (CVD) is increased in the endocrine-metabolic condition polycystic ovary syndrome (PCOS) which impacts 10-15% females. mechanisms cardiac dysfunction PCOS related to hyperandrogenemia, and androgen receptor (AR) estrogen (ER) activation remain unclear. aim this study was investigate effect treatment on AR ER activation, fatty acid metabolism function a PCOS-prone rodent model. An established model pf metabolic syndrome, controls were treated with testosterone (T) for 12 weeks. Cardiac assessed using transthoracic doppler echocardiography, lipogenic, AR, other gene protein expression RTPCR SDS-PAGE western blot. animals exhibited left ventricular (LV) hypertrophy, LV mass body weight ratio (551.6 ± 38.85 mg vs 999 96.17 mg, p<0.05) beta-myosin heavy chain (-MHC) compared controls. Systolic evidenced by isovolumetric contraction time (IVCT; 22.5 1.348 msec 28.96 1.248 msec, elevated B-type natriuretic peptide (BNP) T mass, IVCT IVRT but did not exacerbate animals. PPAR-⍺, ER-⍺ reduced both control Testosterone alters associated adverse morphology conditions.