EFFECT OF INSULIN ON GLYCEROL PRODUCTION IN OBESE ADOLESCENTS

Impaired stimulation of glucose metabolism and reduced suppression of lipolytic activity have both been suggested as important defects relat ed to the insulin resistance of adolescent obesity. To further explore the relationship between these abnormalities, we studied seven obese [body mass index (BMI) 35 +/- 2 kg/m(2)] and seven lean (BMI 21 +/- 1 kg/m(2)) adolescents aged 13-15 yr and compared them with nine lean ad ults (aged 21-27 yr, BMI 23 +/- 1 kg/m(2)) during a two-step euglycemi c-hyperinsulinemic clamp in combination with 1) a constant [H-2(5)]gly cerol (1.2 mg.m(-2).min(-1)) infusion to quantify glycerol turnover an d 2) indirect calorimetry to estimate glucose and net lipid oxidation rates. In absolute terms, basal glycerol turnover was increased and su ppression by insulin was impaired in obese adolescents compared with b oth groups of lean subjects (P < 0.01). However, when the rates of gly cerol turnover were adjusted for differences in body fat mass, the rat es were similar in all three groups. Basal plasma free fatty acid (FFA ) concentrations were significantly elevated, and the suppression by p hysiological increments in plasma insulin was impaired in obese adoles cents compared with lean adults (P < 0.05). In parallel with the high circulating FFA levels, net lipid oxidation in the basal state and dur ing the clamp was also elevated in the obese group compared with lean adults. Net lipid oxidation was inversely correlated with glucose oxid ation (r = -0.50, P < 0.01). In conclusion, these data suggest that li polysis is increased in obese adolescents (vs. lean adolescents and ad ults) as a consequence of an enlarged adipose mass rather than altered sensitivity of adipocytes to the suppressing action of insulin.