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Mol Cell Endocrinol. 2001 Jun 30;180(1-2):109-16.

Clinical studies: inhibin in the adult male.

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  • 1MRC Human Reproductive Sciences Unit, Centre for Reproductive Biology, University of Edinburgh, 37 Chalmers Street, EH39ET, Edinburgh, UK.


The current generation of inhibin assays have allowed the demonstration that inhibin B is the long-postulated testicular factor comprising the feedback inhibitory pathway between the testis and FSH secretion. The inverse relationship between inhibin B and FSH secretion is seen in both normal men and in testicular pathologies. Although inhibin B concentrations are increased by gonadotrophin administration, adult secretion is only partly gonadotrophin dependent and appears more closely related to the presence of germ cells. Thus, inhibin B concentrations are maintained at least at 30% of normal following gonadotrophin suppression, but fall to undetectable levels following loss of all germ cells, e.g. by testicular irradiation. The direct positive correlation between inhibin B and sperm concentration in normal men indicates that inhibin B quantitatively reflects the number of spermatozoa being released. Data from studies of infertile men undergoing testicular biopsy is providing information as to the particular stages of spermatogenesis involved. These intercellular relationships may underlie the relative resistance of inhibin B to suppression by some hormonal contraceptive regimens, despite azoospermia being induced. Inhibin B is also present in seminal plasma. There is a far wider range of concentration in seminal plasma than in blood and the significant relationship with sperm concentration indicates that inhibin secretion into the ejaculate is a marker of the functional activity of the seminiferous tubule. This relationship with sperm production may be a useful marker in some contexts, as changes are more dynamic than in the circulating hormone.

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