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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
Summary
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.