Müllerian inhibiting substance, also known as anti-Müllerian hormone, is a glycoprotein hormone involved in reproductive tract development, gonadal differentiation, follicular regulation, and reproductive endocrine signaling. During embryonic development in males, AMH promotes regression of Müllerian ducts, thereby supporting development of male reproductive anatomy.
In females, AMH is produced by ovarian follicles and functions as a regulator of follicular recruitment and maturation. The hormone helps coordinate ovarian reserve signaling and contributes to communication between developing follicles and endocrine regulatory systems. Through these actions, AMH participates in both developmental reproductive differentiation and adult reproductive physiology.
AMH is produced mainly by Sertoli cells in the testes during male fetal development and by granulosa cells of ovarian follicles in females after birth. In women, production is highest in small developing follicles and gradually changes with reproductive aging and follicular dynamics.
The hormone is synthesized as a glycoprotein precursor that undergoes proteolytic processing to form the biologically active signaling molecule. Ovarian production occurs locally within follicular environments where AMH influences follicle recruitment and growth coordination.
AMH production is regulated by gonadal development, follicular maturation status, gonadotropin signaling, reproductive aging, and local ovarian signaling pathways. In females, follicular population dynamics strongly influence circulating concentrations.
AMH acts through serine-threonine kinase receptors belonging to the transforming growth factor-beta receptor family. Receptor activation stimulates SMAD signaling pathways involved in developmental transcription, follicular regulation, and reproductive tissue differentiation. Feedback systems within gonadal tissues help coordinate endocrine reproductive balance and follicular adaptation. Through these integrated reproductive signaling systems, AMH regulates developmental reproductive differentiation, ovarian follicle communication, and gonadal endocrine coordination.
AMH signals via AMHR2 and SMAD1/5/8 to drive Müllerian duct regression embryonically and to modulate follicle dynamics and FSH sensitivity postnatally.
