Visfatin, a new adipokine, facilitates adipogenesis and has insulin-mimetic properties. There are data that hyperglycemia causes an increase in plasma visfatin levels in people with T2DM this increase gets more prominent as the glucose intolerance worsens. The aim of the study was to investigate plasma visafatin, leptin and adiponectin in obese women with normal and impaired glucose tolerance. Thirteen obese women (age: 34.50±2.57 yrs; BMI 35.05±0.57 kg/m2) with normal glucose tolerance (NGT) and 11 age and BMI matched obese women (age: 37.0 2.4734.50±2.57 yrs; BMI 38.20±1.81 kg/m2) with normal fasting and impaired glucose tolerance during oral glucose tolerance test (OGTT) (IGT) were included in the study. Fasting plasma visfatin (EIA Phoenix, ng/ml), adiponectin (Linco RIA, ng/ml), leptin (Linco RIA, ng/ml) and insulin (RIA Inep, mU/l) were measured. OGTT (75 gr of glucose) were performed in all obese women. Insulin sensitivity (M index: mg/kgBW/min) using hyperinsulinemic euglycemic 2hr clamp was measured before and after weight reduction. There was no difference in fasting visfatin between NGT and IGT (68.65±4.78 vs. 73.14±5.22, P>0.05), fasting leptin (36.75±3.79 vs. 32.06±3.79, P>0.05) fasting adiponectin (6.82±1.84 vs. 10.76±4.14, P>0.05) and fasting insulin (17.34±1.44 vs. 19.08±2.65, P>0.05). Insulin sensitivity was reduced in obese women with IGT (5.36±0.63 vs. 2.81±0.39, P<0.05) while waist circumference were greater in the same subgroup of obese women (101.07±3.12 vs. 113.18±3.60, P<0.05). There was significant correlation between M index and waist in obese women (r=−0.67, P<0.05). In conclusion, decreased insulin sensitivity is confirmed in severe obese women with IGT. Our data suggest that impairment in insulin sensitivity precede change in adipocytokines during development of type 2 diabetes in obesity.