ECE2011 Poster Presentations Female reproduction (39 abstracts)
1UMF Gr.T.Popa, Iasi, Romania; 2UMF Carol Davilla, Bucuresti, Romania.
Introduction: Polycystic ovary syndrome (PCOS) have an increased rate of metabolic syndrome (MS). Many studies have proved that adiponectin is closely associated with MS and participate in the disturbances of gonadal axis. The aim of the study was to evaluate the association of adiponectin levels with MS in PCOS.
Patients and methods: Study group included 38 patients with PCOS (Rotterdam criteria) compared to 30 healthy volunteers age and sex matched, all with BMI>25 kg/m2. Blood pressure (BP), waist circumference, serum adiponectin, fasting glucose, HOMA, lipids levels were performed in all subjects.
Results: In the PCOS group, adiponectin was lower than in the control group, but the difference was not significant (P=0.2). There were no differences between adiponectin values in overweight versus obese women with PCOS (P=0.15), but the difference was significant in the non-PCOS group (P=0.018). Metabolic syndrome was more frequent in PCOS patients, but the difference was not significant (58 vs 46%); in women with MS adiponectin levels were lower, the difference being significant (P=0.012 in control group; P=0.014 in PCOS group). Adiponectin levels were negatively correlated with waist circumference, fasting glucose, triglycerides, and diastolic BP, and positively correlated with HDL. In both groups, adiponectin levels were significantly lower in women with abdominal obesity (P<0.05) and in older women (>35 years old; P<0.03). Insulin resistance had a significant negative correlation with adiponectin in PCOS subjects (r=−0.446) but not in the normal group (r=−0.08).
Discussion: Our results are similar to those of the literature. We presume that adiponectin was not significantly lower in PCOS because both groups had BMI>25 kg/m2. Despite the similar values, MS was more frequent in PCOS. Our results suggest that adiponectin is an independent risk factor for MS and probably involved in PCOS pathogenesis.