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This version published online on August 22, 2006
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2006-0669
A more recent version of this article appeared on November 1, 2006
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Submitted on March 27, 2006
Accepted on August 14, 2006

Serum INSL3 Levels during Puberty in Healthy Boys and Boys with Klinefelter Syndrome

Anne M. Wikström*, Katrine Bay, Matti Hero, Anna-Maria Andersson, and Leo Dunkel

Hospital for Children and Adolescents, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland; University Department of Growth and Reproduction, Rigshospitalet, Copenhagen, Denmark; Department of Pediatrics, Kuopio University Hospital, University of Kuopio, Kuopio, Finland

* To whom correspondence should be addressed. E-mail: anne.wikstrom{at}fimnet.fi.

Context. Levels of the Leydig cell-specific hormone INSL3 are incompletely characterized in boys during pubertal development.

Objective. To characterize changes in INSL3 levels during spontaneous puberty in healthy boys, in boys with aromatase inhibitor-induced hypergonadotropic hyperandrogenism, and in boys with Leydig cell dysfunction.

Design. Prospective clinical study.

Setting. University central hospital, pediatric endocrinology outpatient clinic.

Patients. 30 healthy boys with idiopathic short stature (ISS) aged 9.0-14.5 yr; 14 boys with Klinefelter syndrome (KS) aged 10-13.9 yr.

Intervention. In ISS boys, aromatase inhibitor letrozole or placebo for 24 months.

Main outcome measures. Serum INSL3 levels in relation to bone age, Tanner pubertal stages, and LH and testosterone levels.

Results. Onset of puberty was associated with a significant increase in INSL3 levels from 0.06 ± 0.01 ng/mL at Tanner G1 to 0.32 ± 0.16 ng/mL at G2 (P < 0.0001). Adult INSL3 levels (≥ 0.55 ng/mL) were attained at bone age 13-14 yr. ISS boys with letrozole-induced hypergonadotropic hyperandrogenism had, after 12 months of therapy, higher INSL3 levels than did placebo-treated (0.85 ± 0.54 ng/mL vs. 0.26 ± 0.17 ng/mL, P < 0.01). In KS boys during spontaneous puberty, after an initial increase similar to that in healthy boys INSL3 concentrations leveled off despite hyperstimulation by LH. Positive correlations occurred between S-INSL3 and S-LH, and between S-INSL3 and S-testosterone levels in all three groups (P < 0.0001).

Conclusions. In boys, the Leydig cell-specific hormone INSL3 may serve as a new marker for onset and progression of puberty. Pubertal increase in INSL3 levels seems to depend on LH. In KS subjects, INSL3 concentrations indicate Leydig cell dysfunction from midpuberty onwards.
Key words: INSL3 • puberty • Leydig cells • testosterone • 47 • XXY • Klinefelter syndrome • testicular degeneration • hypergonadotropism




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