Document Detail


Developmental programming of health and disease.
MedLine Citation:
PMID:  16441949     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The environment encountered in fetal and neonatal life exerts a profound influence on physiological function and risk of disease in adult life. Epidemiological evidence suggests that impaired fetal growth followed by rapid catch-up in infancy is a strong predictor of obesity, hypertension, non-insulin-dependent diabetes and CHD. Whilst these associations have been widely accepted to be the product of nutritional factors operating in pregnancy, evidence from human populations to support this assertion is scarce. Animal studies clearly demonstrate that there is a direct association between nutrient imbalance in fetal life and later disease states, including hypertension, diabetes, obesity and renal disease. These associations are independent of changes in fetal growth rates. Experimental studies examining the impact of micro- or macronutrient restriction and excess in rodent pregnancy provide clues to the mechanisms that link fetal nutrition to permanent physiological changes that promote disease. Exposure to glucocorticoids in early life appears to be an important consequence of nutrient imbalance and may lead to alterations in gene expression that have major effects on tissue development and function. Epigenetic mechanisms, including DNA methylation, may also be important processes in early-life programming.
Authors:
Simon C Langley-Evans
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Publication Detail:
Type:  Lectures    
Journal Detail:
Title:  The Proceedings of the Nutrition Society     Volume:  65     ISSN:  0029-6651     ISO Abbreviation:  Proc Nutr Soc     Publication Date:  2006 Feb 
Date Detail:
Created Date:  2006-01-30     Completed Date:  2006-05-22     Revised Date:  2013-06-07    
Medline Journal Info:
Nlm Unique ID:  7505881     Medline TA:  Proc Nutr Soc     Country:  England    
Other Details:
Languages:  eng     Pagination:  97-105     Citation Subset:  IM    
Affiliation:
School of Bioscience, University of Nottingham, Loughborough, UK. Simone.Langley-Evans@Nottingham.ac.uk
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MeSH Terms
Descriptor/Qualifier:
Animals
Diet*
Disease Models, Animal
Female
Fetal Development / physiology*
Gene Expression Regulation, Developmental
Humans
Maternal Exposure
Maternal Nutritional Physiological Phenomena*
Models, Animal
Models, Biological
Pregnancy
Prenatal Exposure Delayed Effects*
Grant Support
ID/Acronym/Agency:
PG/02/047/13752//British Heart Foundation; PG/03/034/15234//British Heart Foundation; PG/04/017/16752//British Heart Foundation
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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