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.
459-467
Bertram, Caroline E.
7cf2f298-1d96-4966-85e5-1f41806905e2
Hanson, Mark A.
1952fad1-abc7-4284-a0bc-a7eb31f70a3f
2002
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), .
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.
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Published date: 2002
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Local EPrints ID: 25251
URI: http://eprints.soton.ac.uk/id/eprint/25251
ISSN: 0022-4251
PURE UUID: 3976770e-eebf-4cd5-94f4-86e173859ef6
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Date deposited: 07 Apr 2006
Last modified: 23 Jul 2022 01:47
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Author:
Caroline E. Bertram
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