Searchable abstracts of presentations at key conferences in endocrinology

ea0038p364 | Reproduction | SFEBES2015

Use of an animal model to identify the origin and validity of the testicular dysgenesis syndrome hypothesis in humans

van den Driesche Sander , Kilcoyne Karen , Wagner Ida , Boyle Ashley , McKinnell Chris , Macpherson Sheila , Mitchell Rod , Sharpe Richard

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...

ea0031p292 | Pituitary | SFEBES2013

Perinatal origins of adult Leydig cells and function: role of developmental androgens

Kilcoyne Karen , Atanossova Nina , Franca Luiz Renato de , Lara Nathalia , Gendt Karel De , Verhoeven Guido , McKinnell Chris , Macpherson Sheila , Driesche Sander van den , Smith Lee , Sharpe Richard M

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...

ea0028oc4.5 | Steroid | SFEBES2012

A novel repressor mechanism regulating fetal Leydig cell steroidogenesis, perturbation of which results in masculinization disorders

van den Driesche Sander , Walker Marion , McKinnell Chris , Scott Hayley , Eddie Sharon , Seckl Jonathan , Drake Amanda , Lee Smith , Anderson Richard , Sharpe Richard

Fetal Leydig cell (LC) dysfunction leads to human male reproductive disorders (‘testicular dysgenesis syndrome’; TDS) that manifest at birth (cryptorchidism, hypospadias) or in young adulthood (low sperm count, testicular germ cell cancer). The factors regulating fetal LC function in early gestation are unknown, but can be disrupted in rats by environmental chemicals (e.g. dibutyl phthalate (DBP)). We identify a novel repressor mechanism that explains this vulnerabil...

ea0028p282 | Reproduction | SFEBES2012

The effects of di(n-butyl) phthalate (DBP) exposure on testis cell development/function in human fetal testis xenografts

Mitchell Rod , Childs Andrew , Anderson Richard , van den Driesche Sander , McKinnell Chris , MacPherson Sheila , Wallace W , Kelnar Chris , Saunders Philippa , Sharpe Richard

Background: Endocrine disruption in the human fetal testis by environmental agents has been proposed as a possible cause of testicular dysgenesis syndrome (TDS) comprising male reproductive disorders such as testicular germ cell tumours (TGCT), cryptorchidism, hypospadias and low sperm counts. Exposure of fetal rats to the widely used plasticizer di(n-butyl) phthalate (DBP) results in a TDS-like syndrome due to a reduction in testosterone production. Whether such effects also ...