Document Detail


Experimental models of developmental programming: consequences of exposure to an energy rich diet during development.
MedLine Citation:
PMID:  15695245     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Studies in both humans and experimental animals addressing the 'Fetal Origins of Adult Disease' hypothesis have established a relationship between an adverse intrauterine environment and offspring disease in adult life. This phenomenon, termed 'fetal programming' describes a process whereby a stimulus in utero establishes a permanent response in the fetus leading to enhanced susceptibility to later disease. However, the environment, during periods of developmental plasticity in postnatal life, can also 'programme' function. Thus, the terms 'developmental programming' and the 'Developmental Origins of Adult Health and Disease' are preferentially utilized. The 'Thrifty Phenotype' hypothesis explained the association between insufficient in utero nutrition and the later development of Type 2 diabetes. Most recently the 'Predictive Adaptive Response' hypothesis proposes that the degree of mismatch between the pre- and postnatal environments is an important determinant of subsequent disease. Epidemiological studies have indicated that fetal growth restriction correlates with later disease, implying that fetal nutritional deprivation is a strong programming stimulus. This prompted the development of experimental animal models using controlled maternal calorie, protein or macronutrient deficiency during key periods of gestation. However, in many societies, maternal and postnatal nutrition are either sufficient or excessive. Here, we examine findings from a range of nutritional studies examining maternal and/or postnatal nutritional excess. There is supportive evidence from a limited number of studies to test the 'Predictive Adaptive Response' hypothesis. These suggest that maternal over-nutrition is deleterious to the health of offspring and can result in a phenotype of the offspring that is characteristic of metabolic syndrome.
Authors:
James A Armitage; Paul D Taylor; Lucilla Poston
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2005-02-03
Journal Detail:
Title:  The Journal of physiology     Volume:  565     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2005 May 
Date Detail:
Created Date:  2005-05-18     Completed Date:  2005-08-16     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  3-8     Citation Subset:  IM    
Affiliation:
Maternal and Fetal Research Unit, Division of Reproductive Health, Endocrinology and Development, GKT School of Medicine, St Thomas' Hospital, Lambeth Palace Road, London SE1 7EH, UK. james.armitage@kcl.ac.uk
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological
Animals
Cardiovascular System / embryology,  physiopathology
Diet
Disease Models, Animal
Energy Metabolism*
Female
Humans
Maternal Exposure / adverse effects
Metabolic Syndrome X / embryology,  etiology,  physiopathology
Models, Animal
Models, Biological
Obesity / embryology*,  etiology,  physiopathology*
Pregnancy
Prenatal Exposure Delayed Effects*
Prenatal Nutritional Physiological Phenomena*
Comments/Corrections
Comment In:
J Physiol. 2005 May 15;565(Pt 1):1   [PMID:  15790658 ]

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


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