The possible role of AMH in shortening the gubernacular cord in testicular descent: A reappraisal of the evidence

Abstract

Background/aim: Anti-Müllerian hormone (AMH), also called Müllerian inhibiting substance (MIS), is glycoprotein hormone secreted by the fetal Sertoli cells to regulate regression of the Müllerian ducts, the anlagen of the uterus, fallopian tubes, and upper vagina. After its existence was predicted in 1946 and its isolation and purification in the 1970's, a huge amount of information has been gathered on its molecular biology and function in the last 30-40years. Once thought to be a locally acting factor in the male fetus during sexual differentiation, it is now recognized as an endocrine hormone present in both sexes and with functions throughout life. One of the remaining controversies is the possible role of AMH during fetal testicular descent. In the human with aberrant AMH function, the boy has cryptorchidism with persistent Müllerian duct syndrome (PMDS), where the testes are often intraabdominal and on an abnormally long gubernacular cord. By contrast, in rodent models knockout of the AMH gene does not cause cryptorchidism.

Methods/results: In this review we examined the evidence in the literature for and against a role for AMH in testicular descent and considered the implications of the different anatomy of the gubernacular cord in rodents versus children.

Conclusion: We conclude that AMH may have a role in shortening the gubernacular cord in humans which is concealed in rodent models by differences in anatomy of the gubernacular cord in rodents. The controversy could be resolved by re-examination of the gubernacular cord in boys with PMDS and mice with AMHKO.

Type of study: Review.

Level of evidence: V.

Keywords: AMH; Anti-Mullerian hormone; Human; MIS; Mullerian inhibiting substance; PMDS; Persistent Mullerian duct syndrome; Rodent.