title: Effect of short-term testosterone treatment on leptin concentrations in boys with pubertal delay.
abstract: Testosterone administration increases growth hormone (GH) secretion and decreases the plasma leptin concentration in men. We evaluated the effect of increased GH secretion due to short-term testosterone treatment on leptin concentrations. Ten boys aged 14.8 +/- 0.2 (mean +/- SE) years with transient GH deficiency caused by pubertal delay were evaluated before and after (3 months) 4 intramuscular injections of 100 mg testosterone heptylate, given at 15-day intervals. The leptin concentration decreased from 5.4 +/- 1.3 to 3. 6 +/- 1.1 microgram/l (p < 0.001), despite a weight gain of 3.4 +/- 0.5 kg. There were significant increases in body mass index (BMI), from -0.2 +/- 0.5 to 0.2 +/- 0.5 SD, p < 0.005, in GH peak after stimulation test, from 6.3 +/- 0.5 to 21.7 +/- 2.9 microgram/l, p < 0. 0003, in plasma testosterone, from 0.6 +/- 0.1 to 6.5 +/- 1.3 microgram/l, p < 0.001, in insulin-like growth factor-I (IGF-I), from 152 +/- 21 to 330 +/- 30 microgram/l, p < 0.0001, and in IGF-binding protein-3 (IGFBP-3), from 4.2 +/- 0.5 to 5.4 +/- 0.4 mg/l, p < 0.01. But there were no changes in blood glucose (4.7 +/- 0.1 and 4.8 +/- 0.1 mmol/l), or plasma fasting insulin (9.0 +/- 1.2 and 8.1 +/- 1.3 mIU/l). The leptin concentrations were positively correlated with the BMI before (p < 0.03) and after (p < 0.04) testosterone, but not with the GH peak after stimulation, or with plasma testosterone, IGF-I or IGFBP-3. The leptin and insulin concentrations after testosterone treatment were positively correlated (p < 0.04). Thus, short-term testosterone treatment of boys with pubertal delay decreases their leptin concentrations. The lack of correlation with GH secretion or with its changes, despite the dramatic increase in GH secretion, and the lack of change in insulin are additional features suggesting that testosterone increases the leptin concentration mainly by an effect on adipose tissue.
authors.affiliation: Pediatric Endocrinology Department, Université René Descartes and Hôpital Necker-Enfants Malades, Assistance Publique-Hôpitaux de Paris, Paris, France.
authors.forename: L
authors.initials: L
authors.lastname: Adan
authors.forename: L
authors.initials: L
authors.lastname: Bussières
authors.forename: C
authors.initials: C
authors.lastname: Trivin
authors.forename: J C
authors.initials: JC
authors.lastname: Souberbielle
authors.forename: R
authors.initials: R
authors.lastname: Brauner
mesh_terms: D000293:Adolescent; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D019382:Human Growth Hormone / Q000097:blood / Q000172:deficiency; D006801:Humans; D007273:Injections, Intramuscular; D007328:Insulin / Q000097:blood; D018972:Insulin-Like Growth Factor Binding Protein 3 / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D020738:Leptin / Q000378:metabolism*; D008297:Male; D011628:Puberty, Delayed / Q000097:blood* / Q000188:drug therapy*; D013739:Testosterone / Q000008:administration & dosage / Q000097:blood / Q000627:therapeutic use*; D015430:Weight Gain
chemical_list: D001786:Blood Glucose; D007328:Insulin; D018972:Insulin-Like Growth Factor Binding Protein 3; D020738:Leptin; D019382:Human Growth Hormone; D013739:Testosterone; D007334:Insulin-Like Growth Factor I