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Prenatal programming of postnatal endocrine responses by glucocorticoids

Caroline E Bertram1, Mark A Hanson

  • 1Centre for Fetal Origins of Adult Disease, Mailpoint 887, Princess Anne Hospital, Coxford Road, Southampton SO16 5YA, UK. c.bertram@soton.ac.uk

Reproduction (Cambridge, England)
|October 4, 2002
PubMed

Insights

Prenatal exposure to glucocorticoids, driven by poor maternal nutrition, may program adult diseases like hypertension and diabetes. This programming affects the hypothalamo-pituitary-adrenal (HPA) axis and related gene expression.

Area of Science:

  • Endocrinology
  • Developmental Biology
  • Epidemiology

Background:

  • Epidemiological studies suggest adult metabolic syndrome risks, including hypertension and diabetes, are established during fetal development.
  • Reduced fetal nutrient supply due to placental issues or maternal malnutrition is a key implicated factor.
  • Excess prenatal glucocorticoid exposure is hypothesized to restrict fetal growth and permanently alter systems.

Purpose of the Study:

  • To review the effects of in utero glucocorticoid exposure on postnatal hypothalamo-pituitary-adrenal (HPA) axis activity.
  • To discuss the physiological consequences and molecular mechanisms of this developmental programming.
  • To examine data from both human and experimental animal studies.

Main Methods:

  • Literature review focusing on epidemiological data and experimental studies.
  • Analysis of research on endogenous and exogenous glucocorticoid exposure during gestation.
  • Examination of molecular and cellular mechanisms involved in programming.

Main Results:

  • Prenatal glucocorticoid exposure impacts postnatal HPA axis activity.
  • This exposure can lead to permanent alterations in cardiovascular, endocrine, and metabolic systems.
  • Key targets for programming include the HPA axis and specific gene expressions.

Conclusions:

  • In utero glucocorticoid exposure is a significant factor in developmental programming of disease risk.
  • The hypothalamo-pituitary-adrenal (HPA) axis is a primary target, alongside glucocorticoid receptor and 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) gene expression.

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