Dihydrotestosterone Treatment in Adolescents with Delayed Puberty: Does it Explain Insulin Resistance of Puberty?

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Abstract
Puberty is characterized by temporary insulin resistance, which subsides with the completion of pubertal development. This insulin resistance is manifested by lower rates of insulin- stimulated glucose metabolism and compensatory hyperinsu- linemia in pubertal compared with prepubertal children. Whether 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 treat- ment in adolescents with delayed puberty was not associated with the deterioration of insulin action. The present investi- gation evaluated the effects of 4 months of dihydrotestoster- one administration (50 mg im every 2 wk) on body composi- tion, glucose, fat, and protein metabolism, and insulin sensitivity. Ten adolescents with delayed puberty were eval- uated before and after 4 months of DHT administration. Body composition was assessed by dual energy x-ray absorptiom- etry. Insulin-stimulated glucose metabolism was measured during a 3-h hyperinsulinemic (40 mU/m2min)-euglycemic clamp procedure. Lipolysis and proteolysis were evaluated by stable isotopes of (2H5)glycerol and (1- 13 C)leucine. After 4 months of dihydrotestosterone treatment, height, weight, and fat free mass increased and percentage of body fat decreased. IGF-I and nocturnal GH levels did not change. There was no significant change in insulin-stimulated glucose metabolism (57.2 3.9 vs. 58.3 3.9 mol/kgmin). Total body proteolysis and lipolysis did not change. In summary, based on the present and past studies, we conclude that during puberty insulin resistance/hyperinsulinemia is not attributable to go- nadal sex steroids in boys. (J Clin Endocrinol Metab 86: 4881- 4886, 2001)

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