PS 016 Predicting type 2 diabetes

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PS 016 Predicting type 2 diabetes 376 The beta cell and insulin resistance in polycystic ovary syndrome: new insights into the origins and prevention of type 2 diabetes J. Tomlinson1, A. Mari2, A. Tura2, K. Bond3, E. Stenhouse4, R.P. Vincent5, J. Pinkney6; 1 Pool Health Centre, Redruth, Cornwall, UK, 2Institute of Biomedical Engineering of the Italian National Research Council, University of Padua, Italy, 3Research and Development, Royal Cornwall Hospital, Truro, 4 School of Nursing and Midwifery, University of Plymouth, 5Clinical Biochemistry, King's College Hospital, London, 6Peninsula Schools of Medicine and Dentistry, University of Plymouth, UK. Background and aims: Polycystic Ovary Syndrome is a risk factor for type 2 diabetes (T2D) and cardiovascular disease (CVD) but the mechanisms are poorly understood. The aim of this study was to investigate how the interplay of insulin secretion and action results in glucose dysregulation in PCOS. Materials and methods: 48 non-diabetic lean and obese women with PCOS (Rotterdam criteria) and 53 BMI-matched controls were studied. Insulin secretion was calculated by a model of insulin secretion and beta cell function from glucose and C-peptide levels, and Insulin Sensitivity Index (ISI) by the method of Matsuda, from a 6-point, 2 hour, 75 g oral glucose challenge. Adiposity was measured by bioimpedance and anthropometry. Results: 1) Women with PCOS and controls were well matched for BMI (mean [SD]28.83 [6.98] vs 29.42 [7.17] kg/m2; p=0.68) and there was no difference in Beta Cell Glucose Sensitivity (BCGS), which is the mean slope of the dose-response function, representing the static relationship between glucose and insulin secretion (median [IQR] 83.3 [62.2-131.9] vs 102.4 [64.1-145.8] pmol/min/mL/mmol; p=0.57). 2) ISI was strongly related to BMI category (35) (ANOVA; p< 0.001), and waist circumference (WC) and visceral fat (VF) (r=0.500.58; p