Dihydrotestosterone treatment in adolescents with delayed puberty: Does itexplain insulin resistance of puberty?

Puberty is characterized by temporary insulin resistance, which subsides wi th the completion of pubertal development. This insulin resistance is manif ested by lower rates of insulin-stimulated glucose metabolism and compensat ory hyperinsulinemia in pubertal compared with prepubertal children. Whethe r or not pubertal insulin resistance is the result of sex steroids or GH or a combination of both has been investigated in our laboratory. Previously, we demonstrated that T treatment in adolescents with delayed puberty was n ot associated with the deterioration of insulin action. The present investi gation evaluated the effects of 4 months of dihydrotestosterone administrat ion (50 mg im every 2 wk) on body composition, glucose, fat, and protein me tabolism, and insulin sensitivity. Ten adolescents with delayed puberty wer e evaluated before and after 4 months of DHT administration. Body compositi on was assessed by dual energy x-ray absorptiometry. Insulin-stimulated glu cose metabolism was measured during a 3-h hyperinsulinemic (40 mU/m(2).min) -euglycemic clamp procedure. Lipolysis and proteolysis were evaluated by st able isotopes of [H-2(5)]glycerol and [1-C-13]leucine. After 4 months of di hydrotestosterone treatment, height, weight, and fat free mass increased an d percentage of body fat decreased. IGF-I and nocturnal GH levels did not c hange. There was no significant change in insulin-stimulated glucose metabo lism (57.2 +/- 3.9 vs. 58.3 +/- 3.9 mu mol/kg.min). Total body proteolysis and lipolysis did not change. In summary, based on the present and past stu dies, we conclude that during puberty insulin resistance/hyperinsulinemia i s not attributable to gonadal sex steroids in boys.