Abstract

Objective: Inhibin is a glycoprotein hormone of gonadal origin which was first identified by its ability to negatively regulate FSH. The first specific assay for the measurement of serum inhibin B was available in 1996. After the first demonstration that inhibin B is the physiologically relevant inhibin form in man, this assay was used to study the changes in serum inhibin B levels in a number of pathophysiological conditions. In childhood, Sertoli cell proliferation and Follicle stimulating hormone (FSH) control inhibin activity, germ cells are a major determinant of inhibin B production in adulthood. After puberty, in the presence of FSH, the prime regulator of inhibin B levels is the spermatogenic status and inhibin B production is directly proportional to the ‘amount’ of spermatogenesis, as shown by the direct correlation between serum inhibin B and sperm count. Once full spermatogenesis is ongoing, changes in inhibin B levels reflect mainly the status of germ cell proliferation and development and depend only secondarily on FSH. Spermatogenic activity requires sufficient testosterone (T) concentration. Testosterone is produced by the Leydig cells under the influence of luteinizing hormone (LH). In the adult, serum inhibin B shows a clear diurnal variation closely related to that of testosterone.

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