Inhibin (and activin)
Also known as: inhibin A, inhibin B, activin
Glycoprotein hormones of the TGF-β family made by granulosa and Sertoli cells (and the placenta) that selectively suppress pituitary FSH secretion, allowing FSH and LH to be regulated independently.
Overview
Inhibins are dimers of a common α-subunit with a βA (inhibin A) or βB (inhibin B) subunit. Inhibin B comes from granulosa cells of small antral follicles in the follicular phase and from Sertoli cells in men, where it reflects the mass of active spermatogenesis. Inhibin A comes from the dominant follicle, the corpus luteum and the placenta.
Inhibins antagonise activins (dimers of β subunits), which stimulate FSH synthesis in gonadotrophs; follistatin binds activin. Because inhibin suppresses FSH but not LH, falling inhibin B with declining follicle numbers explains why FSH rises before LH in the perimenopause.
- Location
Source: granulosa cells, corpus luteum and placenta (inhibin A/B); Sertoli cells (inhibin B). Target: gonadotrophs of the anterior pituitary.
Function
- Selectively inhibits FSH secretion.
- Acts locally within the gonad as a paracrine regulator.
- Physiology
Class: glycoprotein (TGF-β superfamily). Mechanism: binds betaglycan and blocks activin receptor (serine/threonine kinase) signalling.
- Regulation
FSH stimulates inhibin secretion (closing a negative-feedback loop); LH/hCG stimulates luteal and placental inhibin A.
Clinical significance
Clinical markers
Low inhibin B with high FSH indicates impaired spermatogenesis or diminished ovarian reserve. Inhibin A is part of second-trimester quadruple screening (raised in trisomy 21). Inhibin is a tumour marker for ovarian granulosa-cell tumours.
Compiled from standard anatomy and physiology references — see the Endocrine System sources. For education only; not medical advice.