CorpusHuman Anatomy
EndocrineHormone

Anti-Müllerian hormone (AMH)

Also known as: AMH, Müllerian-inhibiting substance, MIS

A TGF-β-family glycoprotein from fetal Sertoli cells that causes regression of the Müllerian (paramesonephric) ducts in males; in women it is secreted by small growing follicles and serves as a marker of ovarian reserve.

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Overview

ClassGlycoprotein (TGF-β family)
ReceptorAMHR2 — serine/threonine kinase

In the male fetus, Sertoli cells secrete AMH from about week 7–8; acting through the AMH type II receptor (a serine/threonine kinase receptor), it causes regression of the paramesonephric (Müllerian) ducts, which would otherwise form the uterine tubes, uterus and upper vagina. Sertoli-cell AMH stays high through childhood and falls at puberty as testosterone rises.

In females, AMH is made by granulosa cells of preantral and small antral follicles. It restrains recruitment of primordial follicles and reduces follicle sensitivity to FSH. Because its level reflects the size of the growing follicle pool, serum AMH is a cycle-independent marker of ovarian reserve: it declines steadily with age and becomes undetectable at menopause.

Location

Source: Sertoli cells (fetal and prepubertal testis); granulosa cells of small follicles (ovary). Targets: Müllerian ducts (fetus); ovarian follicles.

Function

  • Regression of the Müllerian ducts in male embryos.
  • Regulation of follicle recruitment in the ovary.
Physiology

Class: glycoprotein dimer (TGF-β superfamily). Receptor: AMHR2 — serine/threonine kinase.

Regulation

Largely constitutive; in males suppressed by rising intratesticular testosterone at puberty; in females proportional to the number of small growing follicles.

Clinical significance

Ovarian reserve and PCOS

AMH predicts the response to ovarian stimulation in IVF; it is high in PCOS (many small follicles) and low in diminished reserve and premature ovarian insufficiency. It does not reliably predict natural fertility.

Persistent Müllerian duct syndrome

Mutations in AMH or AMHR2 leave a uterus and tubes in otherwise normally virilised 46,XY males, often found during surgery for undescended testes or inguinal hernia.

Compiled from standard anatomy and physiology references — see the Endocrine System sources. For education only; not medical advice.