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Table of Contents
Vol. 19, No. 2, 2010
Issue release date: February 2010
Section title: Review

Open Access Gateway

Med Princ Pract 2010;19:87–98

Developmental Origins of Adult Disease

Langley-Evans S.C. · McMullen S.
School of Biosciences, University of Nottingham, Nottingham, UK
email Corresponding Author

Prof. Simon Langley-Evans

School of Biosciences, University of Nottingham, Sutton Bonington

Loughborough, LE12 5RD (UK)

Tel. +44 115 951 6139, Fax +44 115 951 6122

E-Mail simon.langley-evans@nottingham.ac.uk

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Variation in the quality or quantity of nutrients consumed during pregnancy can exert permanent and powerful effects upon the developing fetus. This programming of fetal development is emerging as a new risk factor for non-communicable diseases of adulthood, including coronary heart disease and the metabolic syndrome. Epidemiological studies show that indicators of nutritional deficit in pregnancy are associated with greater risk of diabetes and cardiovascular mortality. The study of programming in relation to disease processes has been advanced by the development of animal models, which have utilized both under- and overfeeding of specific nutrients in pregnancy. Studies of this nature support the nutritional programming hypothesis and provide tools with which to examine the mechanisms through which programming may occur. Studies of animals subject to undernutrition in utero generally exhibit changes in the structure of key organs, such as the kidney and pancreas. These effects are consistent with the concept that programming influences remodel the development of organs. The causal pathways which extend from tissue remodelling to disease processes are relatively well characterised. In contrast, the processes which drive disordered organ development are poorly understood. It is noteworthy that minor perturbation of maternal nutritional status can programme fetal development. It is suggested therefore that programming is a product of altered expression of key genes. This drives the tissue remodelling response and future disease risk.

© 2010 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Review

Received: April 08, 2009
Accepted: September 02, 2009
Published online: February 04, 2010
Issue release date: February 2010

Number of Print Pages: 12
Number of Figures: 3
Number of Tables: 0

ISSN: 1011-7571 (Print)
eISSN: 1423-0151 (Online)

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