To study the initial period of fat deposition in human obesity, we measured glycerol turnover in 12 children of 135–253% ideal body weight, who had continuously gained weight since the onset of obesity 2–9 yr previously. Hyperinsulinemia developed in these children depending on obesity duration (r = 0.74, P < 0.01). Whole-body glycerol production was twofold greater in the obese children (311 vs. 156 μmol·min−1P < 0.01) and correlated with body fat (r = 0.67, P < 0.005). Normalization of glycerol flux to fat mass revealed that the rate of triglyceride hydrolysis was in fact lower in the adipose tissue of obese children (9.4 vs. 17.7 μmol·min−1/kg body fat) and correlated with plasma insulin (r = 0.64, P < 0.005). Euglycemic insulin clamps showed that the response of glycerol production to a unit increment in plasma insulin concentration was increased in obese children, suggesting increased insulin sensitivity of adipose tissue. As a direct consequence (r = 0.67, P < 0.025) of their elevated plasma glycerol concentration (65 ± 4 vs. 37 ± 2 μM, P < 0.05) obese children had an increased glycerol utilization by the whole body, as well as per unit of lean body mass (9.1 ± 1 vs. 6.5 ± 0.9 μmoles·min− lean body mass−1P < 0.025).

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