The University of Southampton
University of Southampton Institutional Repository

Prenatal programming of postnatal endocrine responses by glucocorticoids

Prenatal programming of postnatal endocrine responses by glucocorticoids
Prenatal programming of postnatal endocrine responses by glucocorticoids
Epidemiological studies have led to the hypothesis that a major component of the risk of diseases such as hypertension, coronary heart disease and non-insulin-dependent diabetes (the ‘metabolic syndrome’) is established before birth. Although the underlying mechanisms of this ‘programming’ of disease have not yet been conclusively determined, a reduced fetal nutrient supply as a consequence of poor placental function or unbalanced maternal nutrition is strongly implicated. It has been proposed that one outcome of suboptimal nutrition is exposure of the fetus to excess glucocorticoids, which restrict fetal growth and programme permanent alterations in its cardiovascular, endocrine and metabolic systems. This review focuses on the effects of endogenous and exogenous glucocorticoid exposure in utero on postnatal hypothalamo–pituitary–adrenal (HPA) axis activity, both in humans and experimental animals. The physiological consequences and proposed underlying molecular and cellular mechanisms are discussed. Current data indicate that key targets for programming may include not only the HPA axis but also glucocorticoid receptor gene and 11b-hydroxysteroid dehydrogenase type 2 (11bHSD2) gene expression in a range of tissues.
0022-4251
459-467
Bertram, Caroline E.
7cf2f298-1d96-4966-85e5-1f41806905e2
Hanson, Mark A.
1952fad1-abc7-4284-a0bc-a7eb31f70a3f
Bertram, Caroline E.
7cf2f298-1d96-4966-85e5-1f41806905e2
Hanson, Mark A.
1952fad1-abc7-4284-a0bc-a7eb31f70a3f

Bertram, Caroline E. and Hanson, Mark A. (2002) Prenatal programming of postnatal endocrine responses by glucocorticoids. Reproduction, 124 (4), 459-467.

Record type: Article

Abstract

Epidemiological studies have led to the hypothesis that a major component of the risk of diseases such as hypertension, coronary heart disease and non-insulin-dependent diabetes (the ‘metabolic syndrome’) is established before birth. Although the underlying mechanisms of this ‘programming’ of disease have not yet been conclusively determined, a reduced fetal nutrient supply as a consequence of poor placental function or unbalanced maternal nutrition is strongly implicated. It has been proposed that one outcome of suboptimal nutrition is exposure of the fetus to excess glucocorticoids, which restrict fetal growth and programme permanent alterations in its cardiovascular, endocrine and metabolic systems. This review focuses on the effects of endogenous and exogenous glucocorticoid exposure in utero on postnatal hypothalamo–pituitary–adrenal (HPA) axis activity, both in humans and experimental animals. The physiological consequences and proposed underlying molecular and cellular mechanisms are discussed. Current data indicate that key targets for programming may include not only the HPA axis but also glucocorticoid receptor gene and 11b-hydroxysteroid dehydrogenase type 2 (11bHSD2) gene expression in a range of tissues.

Full text not available from this repository.

More information

Published date: 2002

Identifiers

Local EPrints ID: 25251
URI: http://eprints.soton.ac.uk/id/eprint/25251
ISSN: 0022-4251
PURE UUID: 3976770e-eebf-4cd5-94f4-86e173859ef6
ORCID for Mark A. Hanson: ORCID iD orcid.org/0000-0002-6907-613X

Catalogue record

Date deposited: 07 Apr 2006
Last modified: 17 Dec 2019 01:52

Export record

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×