A molecular basis for estrogen-induced cryptorchidism

Serge Nef, Tracey Shipman, Luis F. Parada

Research output: Contribution to journalArticlepeer-review

167 Scopus citations


Male sexual differentiation relies upon testicular secretion of the hormones testosterone, Mullerian inhibiting substance, and insulin-3 (Insl3). Insl3 is responsible for testicular descent through virilization and outgrowth of the embryonic gubernaculum. In mouse, prenatal exposure to 17β-estradiol and the nonsteroidal synthetic estrogen diethylstilbestrol (DES) disturbs the endocrine balance, causing demasculinizing and feminizing effects in the male embryo, including impaired testicular descent (cryptorchidism). In the current study, we show that maternal exposure to estrogens, including 17α- and β-estradiol, as well as DES, specifically down regulates Insl3 expression in embryonic Leydig cells, thereby providing a mechanism for cryptorchidism. These experiments may have implications for the widespread use of estrogenic substances in agriculture and the environment. (C) 2000 Academic Press.

Original languageEnglish (US)
Pages (from-to)354-361
Number of pages8
JournalDevelopmental Biology
Issue number2
StatePublished - Aug 15 2000


  • Cryptorchidism
  • DES
  • Estradiol
  • Estriol
  • Gubernaculum
  • Insl3
  • Ley I-L
  • RLF

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology


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