QT Interval prolongation is common in insulin resistance state obesity. Insulin-induced hyperpolarization might be involved in ventricular repolarization leading to QTc lengthening. Therefore, this study is designated to investigate the relationship between corrected QT interval (QTc) prolongation and insulin resistance in obese adult male subjects. Apparently healthy adult male subjects (n=100) aged between 18-35 years residing in Magway Township were recruited by simple random sampling method. Then all the eligible subjects were categorized into 2 groups: non-obese [body mass index (BMI) 18.5 to 24.9 kg/m2, n= 40] and obese group [BMI ≥ 30.0 kg/m2, n=60] by their anthropometric parameters. Serum fasting glucose was measured by glucose oxidase method. Serum insulin level was determined by Enzyme-Linked Immunosorbent Assay (ELISA). Insulin sensitivity was calculated by Homeostatic Model Assessment (HOMA-IR). The QT interval was measured by routine 12-lead ECG and corrected QT interval (QTc) was calculated according to Bazett’s formula. In the present study, insulin sensitivity (HOMA-IR) was higher in obese subjects (4.64±2.3) than that of non-obese subjects (2.5±0.89) (p< 0.001). There was significant positive correlation between QTc and HOMA-IR (r = 0.41, p< 0.001, n = 100) in this study. HOMA-IR >3.8 was considered as insulin resistance (IR) and QTc > 440ms was regarded as QTc interval prolongation. Insulin resistance was significantly associated with prolonged QTc interval in the study population (X2=7.3, p< 0.05, n=100). Risk of QTc interval prolongation was 3.4 times higher in subjects with IR (Odd ratio = 3.4; 95% confidence interval = 1.37 to 8.45). It was concluded that prolonged QTc interval is associated with insulin resistance state.