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Submitted on January 31, 2006
Accepted on April 10, 2006
Division of Reproductive and Developmental Sciences, MRC Human Reproductive Sciences Unit, Centre for Reproductive Biology, University of Edinburgh, Edinburgh, UK and Family Planning and Well Woman Services, Lothian Health, Edinburgh UK
* To whom correspondence should be addressed. E-mail: richard.anderson{at}ed.ac.uk.
Context. Testicular production of steroids and gametes is under gonadotropin support but there is little information as to the molecular mechanisms by which these are regulated in the human. The testicular response to gonadotropin withdrawal is important for the development of effective contraceptive methods.
Objective. Investigation of expression of genes in the normal human testis reflecting steroidogenesis, Sertoli cell function and spermatogenesis following short-term gonadotropin withdrawal, and the effects of activating testicular progesterone receptors.
Design. Randomized controlled trial.
Setting. Research Institute.
Patients. 30 healthy men.
Interventions. Subjects were randomized to no treatment, gonadotropin suppression by GnRH antagonist (cetrorelix) with testosterone (CT group), or with additional administration of the gestogen desogestrel (CTD group) for 4 weeks before testicular biopsy. Gene expression was quantified by RT-PCR.
Results. Both treatment groups showed similar suppression of gonadotropins and sperm production, and markedly reduced expression of steroidogenic enzymes. Addition of progestogen in the CTD group resulted in reduced expression of 5
-reductase type 1 compared with both controls and the CT group. Inhibin and the spermatocyte marker acrosin binding protein were significantly lower in the CTD but not CT groups compared with controls although did not differ between treated groups. Men who showed greater falls in sperm production also showed reduced expression of these 3 genes but not of the spermatid marker PRM1.
Conclusions. These data provide evidence for direct progestogenic effects on the testis and highlight steroid 5-reduction and disruption of spermiation as important components of the testicular response to gonadotropin withdrawal.
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