Inhibin B in males is produced principally by Sertoli cells under the influence of FSH and is thought to have a role in feedback regulation of FSH. The aims of our study were to investigate how inhibin B changes from birth to late adolescence in boys, to derive reference data and to explore its relation with pubertal stage, FSH and testosterone. Blood samples were collected from (i) 366 boys aged 0--18 years to obtain age-related reference data; (ii) 195 boys who had full pubertal staging; and (iii) a cohort of 15 boys studied longitudinally as they approached and entered early puberty. Dimeric inhibin B was measured by double antibody enzyme-linked immunosorbent assay (ELISA), FSH by immunoradiometric assay (IRA) and testosterone by an extraction radioimmunoassay. Inhibin B was high in infant boys, decreased gradually to a nadir at 6--10 years of age, then increased rapidly in early adolescence to reach a new plateau at 12--17 years. It was detectable in all samples. Age-related reference ranges and data for calculation of SD scores are presented. In prepubertal boys, inhibin B correlated positively with age (P < 0.001), but not with FSH. Inhibin B increased progressively from pubertal stages G1 to G3 but then decreased slightly at stages G4 to G5 (P less-than-or-equal 0.01). At stage G2, inhibin B correlated positively with testosterone (P < 0.01) but not with FSH. From stage G3 onwards, inhibin B correlated inversely with FSH (P < 0.01) but lost its relationship with testosterone. In the cohort of boys studied longitudinally, inhibin B increased progressively prior to pubertal onset and further on entry into early clinical puberty (P < 0.05). Testosterone also increased over this period (P < 0.05) but FSH showed no significant change. The two peaks of inhibin B during infancy and early puberty appear to reflect the two periods of Sertoli cell proliferation in normal human males. During mid-childhood, a relatively constant amount of inhibin B is secreted constitutively. The early FSH-independent increase in inhibin B that precedes clinical puberty and continues to stage G2 may be stimulated by testosterone or other factors from Leydig cells. The inverse relationship between inhibin B and FSH that subsequently develops from mid-puberty onwards is consistent with the establishment of a negative feedback loop at this time.
