Identification of a new mechanism that could underly disorders of foetal testis development

It is well known that perturbations to testis development in foetal life can underpin certain reproductive disorders in males, such as infertility, hypospadias, cryptorchidism and testicular cancer.

New research from the Hudson Institute of Medical Research has discovered a new mechanism in foetal testis development that could be vulnerable to environmental disturbances and could, in turn, have long lasting impacts on male health and fertility.

Previous research has shown that the protein activin A is required for the normal development of the seminiferous cords, the structures in the foetal testis that will eventually become the site of sperm production in the adult. Alterations in activin A can disturb the balance between the gonocytes (the foetal germ cells that will ultimately differentiate into sperm) and the somatic cells that support sperm production, leading to infertility.

Research by Kate Loveland’s group at the Centre for Reproductive Health has now revealed that alterations in activin A impact on the production of androgen within the testis and that this could be a key reason why the testis develops abnormally. Androgens are essential for male development, yet alterations in activin A caused important changes in the amount and type of androgens produced in the foetal testis.

This is important because circulating activin A can be altered by various conditions in pregnant women, including preeclampsia, infection or exposure to certain medications. This work suggests exposure to certain conditions during pregnancy could alter activin A at a key stage of testis development, and this could result in androgen imbalance and disorders of reproduction.  

See the article here