title: Dihydrotestosterone treatment in adolescents with delayed puberty: does it explain insulin resistance of puberty?
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 hyperinsulinemia 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 treatment in adolescents with delayed puberty was not associated with the deterioration of insulin action. The present investigation evaluated the effects of 4 months of dihydrotestosterone administration (50 mg im every 2 wk) on body composition, glucose, fat, and protein metabolism, and insulin sensitivity. Ten adolescents with delayed puberty were evaluated before and after 4 months of DHT administration. Body composition was assessed by dual energy x-ray absorptiometry. Insulin-stimulated glucose metabolism was measured during a 3-h hyperinsulinemic (40 mU/m(2).min)-euglycemic clamp procedure. Lipolysis and proteolysis were evaluated by stable isotopes of [(2)H(5)]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 micromol/kg.min). 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 gonadal sex steroids in boys.
authors.affiliation: Children's Hospital of Pittsburgh, 3705 Fifth Avenue at DeSoto Street, Pittsburgh, PA 15213, USA.
authors.forename: R J
authors.initials: RJ
authors.lastname: Saad
authors.forename: B S
authors.initials: BS
authors.lastname: Keenan
authors.forename: K
authors.initials: K
authors.lastname: Danadian
authors.forename: V D
authors.initials: VD
authors.lastname: Lewy
authors.forename: S A
authors.initials: SA
authors.lastname: Arslanian
mesh_terms: D000293:Adolescent; D001823:Body Composition / Q000187:drug effects; D013196:Dihydrotestosterone / Q000627:therapeutic use*; D004958:Estradiol / Q000502:physiology; D005223:Fats / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D019382:Human Growth Hormone / Q000502:physiology; D006801:Humans; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood; D008297:Male; D011506:Proteins / Q000378:metabolism; D011628:Puberty, Delayed / Q000188:drug therapy* / Q000378:metabolism
chemical_list: D005223:Fats; D008055:Lipids; D011506:Proteins; D013196:Dihydrotestosterone; D019382:Human Growth Hormone; D004958:Estradiol; D005947:Glucose