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Glucocorticoids as mediators of developmental programming effects.

Batbayar Khulan1, Amanda J Drake

  • 1Endocrinology Unit, Centre for Cardiovascular Science, University of Edinburgh, Queen's Medical Research Institute, Edinburgh, UK. kbatbaya@staffmail.ed.ac.uk

Best Practice & Research. Clinical Endocrinology & Metabolism
|September 18, 2012
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Summary
This summary is machine-generated.

Early life exposure to adverse environments, particularly fetal glucocorticoid overexposure, can program adult cardio-metabolic and behavioral disorders. This programming effect, observed in animal models and humans, may involve epigenetic modifications.

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Area of Science:

  • Endocrinology
  • Developmental Biology
  • Epidemiology

Background:

  • Early life programming links adverse environments to adult health risks.
  • Fetal glucocorticoid overexposure is a key hypothesis for this programming.
  • Prenatal glucocorticoid excess in animals impacts cardiovascular, metabolic, and brain development, with transgenerational effects.

Purpose of the Study:

  • To review evidence for glucocorticoid programming in animal models and humans.
  • To explore the mechanisms underlying early life programming by glucocorticoids.

Main Methods:

  • Review of epidemiological studies in humans.
  • Analysis of findings from animal models of prenatal glucocorticoid excess.

Main Results:

  • Human studies suggest prenatal glucocorticoid exposure impacts glucose/insulin homeostasis, blood pressure, and neurodevelopment.
  • Animal studies demonstrate programming effects on multiple physiological systems and the brain.
  • Observed effects can be transmitted across generations.

Conclusions:

  • Prenatal glucocorticoid exposure is implicated in early life programming of adult disorders.
  • Epigenetic modifications are potential mechanisms mediating these programming effects.
  • Further research is needed to elucidate the precise mechanisms.