Background: Hyperinsulinemia is known to increase sympathetic nervous system activity (1), although it is unclear if there is a differential response to hyperinsulinemia in individuals who range from low to normal BMI. Low BMI is an important public health problem in the developing world, and may successful adaptations to a habitually low energy intake may result in different autonomic responses to stress. Approximately 30% of adults in developing world have low BMI (2). We therefore evaluated whether individuals of low BMI had differentiated autonomic nervous response to hyperinsulinemia during controlled laboratory conditions as compared with individuals of normal BMI. Method: 51 young men (aged 18-35 years) were divided into 2 groups based on their body mass index. Normal BMI (n=23; BMI,18.5-24.9 Kg/m2) and the low BMI (n=28; BMI, < 18.5 Kg/m2). All subjects underwent assessment of detailed anthropometry, physical activity levels (PAL) and euglycemic hyperinsulimeic clamp (HEC) (3). Lead II ECG and beat to beat blood pressure (4, 5) was recorded during the HEC. Results: Anthropometric parameters were significantly higher in the normal BMI group as compared to Low BMI group (all P<0.01). The PAL in the 2 groups was comparable. Fasting glucose levels were comparable between the groups. Basal insulin level and steady state plasma insulin values (average of 40 to 120 min) during HEC were significantly higher in normal BMI compared to low BMI group (both p<0.05). However, insulin sensitivity and glucose disposal rates during the HEC were significantly higher in the low BMI group. Heart rate, diastolic BP and systolic blood pressure increased in both the groups with hyperinsulinemia but there were no difference in the magnitude of response between the two groups (Group x Time interaction; NS). LF-RR power (nu) increased and HF-RR power (nu) decreased with hyperinsulinemia, resulting in a significant increase in LF/HF ratio but with no between group differences.The low frequency component of the SBP, increased significantly with hyperinsulinemia and there was a trend towards a reduction in baroreflex sensitivity although this was not statistically significant. Conclusion: Cardiac sympathetic activity to hyperinsulinemia increased in both low and normal BMI groups. However, there were no between group differences. Earlier studies have suggested that insulin sensitivity is a determinant of the sympathetic response to hyperinsulinemia. The fact that the two study groups had similar autonomic responses despite differences in insulin sensitivity, suggests that there are factors other than insulin sensitivity or body composition that determine autonomic responses to hyperinsulinemia.