L. Adan et al., Effect of short-term testosterone treatment on leptin concentrations in boys with pubertal delay, HORMONE RES, 52(3), 1999, pp. 109-112
Testosterone administration increases growth hormone (GH) secretion and dec
reases the plasma leptin concentration in men. We evaluated the effect of i
ncreased GH secretion due to short-term testosterone treatment on leptin co
ncentrations. 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 mu g/l (p < 0.001), despite a weight gain of 3.4 +/- 0.5 kg. T
here 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 mu g/l, p < 0.0003, in plasma testosterone, from 0.
6 +/- 0.1 to 6.5 +/- 1.3 mu g/l, p < 0.001, in insulin-like growth factor-I
(IGF-I), from 152 +/- 21 to 330 +/- 30 mu g/l, p < 0.0001, and in IGF-bind
ing protein-3 (IGFBP-3), from 4.2 +/- 0.5 to 5.4 +/- 0.4 mg/l, p < 0.01. Bu
t 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 mlU/l). The lept
in concentrations were positively correlated with the BMI before (p < 0.03)
and after (p < 0.04) testosterone, but not with the GH peak after stimulat
ion, 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 sec
retion or with its changes, despite the dramatic increase in GH secretion,
and the lack of change in insulin are additional features suggesting that t
estosterone increases the leptin concentration mainly by an effect on adipo
se tissue.