Endocrine Abstracts

From human epidemiological and related studies, there is strong (indirect) evidence that common male reproductive disorders that manifest at birth (cryptorchidism, hypospadias) or in adulthood (low sperm count, low testosterone, primary hypogonadism) may have a common origin in foetal life due to impaired androgen (testosterone) production or action; the so-called testicular dysgenesis syndrome (TDS) hypothesis. Whilst the foetal origin of cryptorchidism and hypospadias is sel...

Fetal events can affect adult testosterone levels but how this occurs is unknown, as adult Leydig cells (ALC) do not differentiate until puberty. Qin et al. 2008 (PLos ONE) identified that chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) is essential postnatally for ALC development. We hypothesized that: i) COUP-TFII+ non-Leydig interstitial cells are progenitors for ALC and are present in the fetal testis, ii) these ‘pr...