Dihydrotestosterone treatment in adolescents with delayed puberty: does it explain insulin resistance of puberty?
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.
Saad
R J
RJ
Children's Hospital of Pittsburgh, 3705 Fifth Avenue at DeSoto Street, Pittsburgh, PA 15213, USA.
Keenan
B S
BS
Danadian
K
K
Lewy
V D
VD
Arslanian
S A
SA
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
D005223:Fats; D008055:Lipids; D011506:Proteins; D013196:Dihydrotestosterone; D019382:Human Growth Hormone; D004958:Estradiol; D005947:Glucose