ECE2015 Eposter Presentations Reproduction, endocrine disruptors and signalling (92 abstracts)
1Clinic of Endocrinology, Diabetes and Metabolic Diseases, Faculty of Medicine, University of Belgrade, Belgrade, Serbia; 2CHC Bezanijska kosa, Belgrade, Serbia; 3IBISS, University of Belgrade, Belgrade, Serbia; 4Clinic of Gynecology and Obstetrics, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
Introduction: Insulin resistance (IR) is a well recognised feature in women with polycystic ovary syndrome (PCOS). The aim of this study was to analyse IR indices obtained from oral glucose tolerance test (OGTT), in different PCOS phenotypes.
Methods: We evaluated 240 PCOS women (PCOS: 24.86±5.97 kg/m2; 25.25±4.98 years) diagnosed using ESHRE/ASRM criteria and 70 BMI-matched healthy women (controls: 26.14±4.86 kg/m2; 30.76±5.82 years). PCOS group was divided into four phenotypes: A (anovulation (ANOV), hyperandrogenism (HA), and polycystic ovary morphology (PCOM)), B (ANOV and HA), C (HA and PCOM), and D (ANOV and PCOM). Phenotype D had lower BMI in comparison to all other phenotypes (P<0.05). Standard OGTT with 75 g glucose was performed in all subjects. IR was estimated by the homeostasis model assessment of IR (HOMA-IR), insulin sensitivity index (ISI), hepatic IR index (HIRI), and insulinogenic index (IGI). Areas under insulin (AUCi) and glucose (AUCg) and their ratio, termed the insulin secretion-sensitivity index-2 (ISSI-2) were calculated.
Results: The whole PCOS group in comparison with controls had higher levels of basal glucose (4.89±0.45 mmol/l vs 4.57±0.50 mmol/l, P=0.003) and insulin (17.16±10.36 mU/l vs 11.95±6.53 mU/l, P<0.001), HOMA-IR (3.64±2.38 vs 2.66±1.48, P<0.001), HIRI (3.98±2.65 vs 2.20±0.85×106, P=0.027), IGI (22.13±15.86 vs 10.31±4.13, P=0.027), AUCg (711.63±153.87 vs 670.68±86.48, P=0.012), AUCi (7847.97±4660.48 vs 4647.80±1665.78, P=0.029), and ISSI-2 (10.83±5.49 vs 6.51±2.14, P=0.019) while ISI (4.50±2.14 vs 6.04±2.71, P=0.032) was lower. Phenotype B had higher levels of basal insulin and HOMA-IR then phenotypes A, C, and D while AUCi, HIRI, ISSI-2 were higher and ISI was lower then in phenotypes C and D. There were no differences in basal glucose, AUCg and IGI between phenotypes.
Conclusion: In our group of women with PCOS, classical hyperandrogenemic phenotype B was characterised with the most exaggerated indices of IR.