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Androgens and the masculinization programming window: human-rodent differences.

Richard M Sharpe1

  • 1MRC Centre for Reproductive Health, The Queen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, U.K.

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|August 12, 2020
PubMed
Summary
This summary is machine-generated.

Testicular dysgenesis syndrome (TDS) in males may originate in fetal development. While environmental chemicals and painkillers can affect fetal development in rats, human studies suggest placental function and maternal factors are more critical for TDS origins.

Keywords:
androgensbackdoor pathwayfetal programmingmasculinizationplacentatesticular dysgenesis syndrome

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Area of Science:

  • Reproductive biology
  • Developmental toxicology
  • Endocrinology

Background:

  • Testicular dysgenesis syndrome (TDS) is a common male reproductive disorder with a potential fetal origin.
  • The masculinization programming window (MPW) is critical for fetal androgen action, influencing both reproductive development and anogenital distance (AGD).
  • Shorter male AGD in rats correlates with induced TDS disorders, serving as a marker for MPW androgen exposure.

Purpose of the Study:

  • To investigate the origins of testicular dysgenesis syndrome (TDS) in humans, comparing findings with rodent models.
  • To evaluate the impact of environmental chemicals and therapeutic agents on fetal androgen production and AGD.
  • To elucidate the differing mechanisms of androgen regulation during the human and rat MPW.

Main Methods:

  • Review of epidemiological studies on maternal exposure to phthalates (DEHP, DBP), pesticides, and paracetamol.
  • Analysis of fetal human testis culture and xenograft models.
  • Comparison of androgen production pathways and regulatory mechanisms between rats and humans during the MPW.

Main Results:

  • Environmental chemicals (DEHP, DBP) and paracetamol can disrupt fetal androgen production and AGD in rats during the MPW.
  • Human studies show mixed results for environmental chemical exposure and AGD, with effects seen at much lower doses than in rats.
  • In human fetal testis models, DEHP/DBP did not reduce testosterone, but therapeutic paracetamol did.
  • Human MPW androgenesis differs from rats, involving human chorionic gonadotrophin and the 'backdoor pathway', with contributions from placenta, liver, and adrenals.

Conclusions:

  • While environmental exposures can induce TDS in rats, their role in human TDS may be less significant than previously thought.
  • Placental dysfunction, influenced by maternal lifestyle and diet, and maternal analgesic use, may be more critical factors in the etiology of human TDS.
  • The distinct endocrine regulation of the human MPW necessitates a re-evaluation of the primary drivers of TDS in males.