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Submitted on August 17, 2005
Accepted on December 27, 2005
University Department of Growth and Reproduction, GR 5064, Rigshospitalet, DK-2100 Copenhagen, Denmark, Prince Henry's Institute of Medical Research and Department of Obstetrics and Gynaecology, Monash University, Monash Medical Center, Monash, Clayton VIC 3168, Australia
* To whom correspondence should be addressed. E-mail: katrine.bay{at}rh.hosp.dk.
Context: Gonadotropic regulation of the testicular Leydig cell hormone insulin-like factor 3 (INSL3) is incompletely characterized.
Objective: To assess the effects of gonadotropin suppression and induced or spontaneous recovery on serum INSL3.
Design and participants: Serum samples from fifteen men enrolled in a short-term study on gonadotropin stimulation, suppression and recovery, and eleven men in a long-term study on gonadotropin suppression and spontaneous recovery, were analyzed for INSL3.
Intervention: Gonadotropins were suppressed by exogenous testosterone and progestin. Recovery was spontaneous or induced with exogenous gonadotropins.
Outcome measure: Serum INSL3 in relation to other reproductive hormones.
Results: Serum INSL3 was not acutely sensitive to gonadotropins. In both studies, INSL3 declined markedly with gonadotropin suppression (6-13.5% baseline, P < 0.05). In the short-term study, hCG partially restored suppressed serum INSL3 within 4 days of their administration (7.5% to 38.3% baseline, P < 0.05), the increase correlating with corresponding increase in serum pro-
C (r=0.82, P < 0.01). FSH did not stimulate the suppressed INSL3. In the long-term study, serum testosterone recovered significantly better (80% baseline) compared with serum INSL3 (38.9% baseline) (P < 0.01), in the presence of fully recovered serum LH.
Conclusions: INSL3 is not sensitive to gonadotropin stimulation in normal men but declines markedly in response to gonadotropin deprivation. After suppression, INSL3 was responsive to hCG 4 days post administration. After long-term suppression, INSL3 did not recover to the same degree as testosterone, suggesting that INSL3 is more sensitive to Leydig cell impairment, compared with testosterone.
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