Objective: To determine whether prepubertal (Tanner I) obese children have diminished peripheral insulin sensitivity (IS) and to determine whether obesity affects the ability of glucose to stimulate its own disposal (glucose effectiveness, GE).
Design: Cross-sectional study of two groups.
Subjects: Seven obese (BMI > 75% for age, 26.1 +/- 2.1 kg/m2, age, 10.9 +/- 0.6 y, mean +/- SE) and six lean (BMI, 15.7 +/- 0.7 kg/m2, age, 10.3 +/- 0.7) children.
Methods: IS and GE by 3 h frequently sampled intravenous glucose tolerance test with 13% [6-6] D2-glucose in the glucose bolus (250 mg/kg), hepatic glucose production using Steele's non steady state equations and hepatic insulin resistance (HR) multiplying by the mean insulin level.
Results: IS was markedly lower (p < 0.01) in the obese group (0.27 +/- 0.08 (pmol l)/min) compared to the lean group (2.23 +/- 1.0 (pmol/l)min) whereas GE was higher (0.021 +/- 0.001 vs 0.015 +/- 0.001/min, p < 0.05). HR was increased in the obese (132 +/- 28 vs 58 +/- 14 mg/kg/min/pmol/l, p < 0.05). Obese children also had increased insulin secretion over the first 19 min (p > 0.01) following glucose although plasma glucose levels were higher (p < 0.01).
Conclusion: These results show that obese prepubertal children have peripheral and hepatic insulin resistance. The increase in GE and insulin secretion may be compensatory responses to these defects in insulin action.