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Related Experiment Videos

Stress hormone and male reproductive function.

Matthew P Hardy1, Hui-Bao Gao, Qiang Dong

  • 1Center for Biomedical Research, Population Council, New York, NY 10021, USA. hardy@popcbr.rockfeller.edu

Cell and Tissue Research
|August 5, 2005
PubMed
Summary

Stress-induced corticosterone (CORT) increases Leydig cell apoptosis, reducing testosterone production. This study investigates CORT

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Area of Science:

  • Endocrinology
  • Reproductive Biology
  • Cell Biology

Background:

  • Leydig cells are the primary source of testosterone in males.
  • Stress increases serum glucocorticoids, inhibiting testosterone biosynthesis.
  • The effect of stress-induced glucocorticoids on Leydig cell numbers via apoptosis is unclear.

Purpose of the Study:

  • To investigate whether excessive glucocorticoid stimulation affects Leydig cell numbers through apoptosis.
  • To explore the role of 11 beta-hydroxysteroid dehydrogenase (11 betaHSD) in modulating glucocorticoid action in Leydig cells.
  • To examine the potential involvement of non-genomic pathways in glucocorticoid-induced Leydig cell suppression.

Main Methods:

  • Exposure of Leydig cells to high corticosterone (CORT) concentrations.

Related Experiment Videos

  • Studies of immobilization stress in rodents.
  • Analysis of 11 beta-hydroxysteroid dehydrogenase (11 betaHSD) expression and activity in Leydig cells.
  • Investigation of NADPH generation and its role in steroidogenesis.
  • Examination of glucocorticoid receptor binding and non-genomic signaling pathways.

    • Main Results:

    • High CORT concentrations increase Leydig cell apoptosis.
    • Stress-induced CORT increases are directly responsible for Leydig cell apoptosis.
    • Leydig cells express 11 betaHSD types 1 and 2, which modulate glucocorticoid receptor access.
    • NADPH generated by 11 betaHSD-1 may potentiate testosterone biosynthesis.
    • High CORT levels under stress can exceed 11 betaHSD's capacity, inhibiting steroidogenesis.
    • Evidence suggests a fast, non-genomic pathway for glucocorticoid action in Leydig cells.

    Conclusions:

    • Stress-induced elevations in corticosterone directly cause Leydig cell apoptosis, contributing to suppressed androgen levels.
    • 11 beta-hydroxysteroid dehydrogenase (11 betaHSD) plays a crucial role in regulating Leydig cell sensitivity to glucocorticoids.
    • Further research into the rapid, non-genomic effects of glucocorticoids on Leydig cells is warranted.