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Nutritional programming of the metabolic syndrome

Michael E Symonds, Sylvain P Sebert, Melanie A Hyatt, Helen Budge, Melanie Healy

Nature Reviews Endocrinology, Volume: 5, Issue: 11, Pages: 604 - 610

Swansea University Author: Melanie Healy

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Abstract

The primary markers of the metabolic syndrome are central obesity, insulin resistance and hypertension. In this review, we consider the effect of changes in maternal nutrition during critical windows in fetal development on an individual's subsequent predisposition to the metabolic syndrome. Th...

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Published in: Nature Reviews Endocrinology
ISSN: 1759-5029 1759-5037
Published: 2009
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URI: https://cronfa.swan.ac.uk/Record/cronfa12192
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spelling 2011-10-01T00:00:00.0000000 v2 12192 2012-07-20 Nutritional programming of the metabolic syndrome 4654b4128fb21d68f98e2abc8538b45a Melanie Healy Melanie Healy true false 2012-07-20 PHAR The primary markers of the metabolic syndrome are central obesity, insulin resistance and hypertension. In this review, we consider the effect of changes in maternal nutrition during critical windows in fetal development on an individual's subsequent predisposition to the metabolic syndrome. The fetal origins of obesity, cardiovascular disease and insulin resistance have been investigated in a wide range of epidemiological and animal studies; these investigations highlight adaptations made by the nutritionally manipulated fetus that aim to maintain energy homeostasis to ensure survival. One consequence of such developmental plasticity may be a long term re-setting of cellular energy homeostasis, most probably via epigenetic modification of genes involved in a number of key regulatory pathways. For example, reduced maternal-fetal nutrition during early gestation to midgestation affects adipose tissue development and adiposity of the fetus by setting an increased number of adipocyte precursor cells. Importantly, clinically relevant adaptations to nutritional challenges in utero may only manifest as primary components of the metabolic syndrome if followed by a period of accelerated growth early in the postnatal period and/or if offspring become obese. Journal Article Nature Reviews Endocrinology 5 11 604 610 1759-5029 1759-5037 30 11 2009 2009-11-30 10.1038/nrendo.2009.195 http://www.nature.com/nrendo/journal/v5/n11/full/nrendo.2009.195.html COLLEGE NANME Pharmacy COLLEGE CODE PHAR Swansea University 2011-10-01T00:00:00.0000000 2012-07-20T11:39:54.4957682 Faculty of Medicine, Health and Life Sciences Swansea University Medical School - Medicine Michael E Symonds 1 Sylvain P Sebert 2 Melanie A Hyatt 3 Helen Budge 4 Melanie Healy 5
title Nutritional programming of the metabolic syndrome
spellingShingle Nutritional programming of the metabolic syndrome
Melanie Healy
title_short Nutritional programming of the metabolic syndrome
title_full Nutritional programming of the metabolic syndrome
title_fullStr Nutritional programming of the metabolic syndrome
title_full_unstemmed Nutritional programming of the metabolic syndrome
title_sort Nutritional programming of the metabolic syndrome
author_id_str_mv 4654b4128fb21d68f98e2abc8538b45a
author_id_fullname_str_mv 4654b4128fb21d68f98e2abc8538b45a_***_Melanie Healy
author Melanie Healy
author2 Michael E Symonds
Sylvain P Sebert
Melanie A Hyatt
Helen Budge
Melanie Healy
format Journal article
container_title Nature Reviews Endocrinology
container_volume 5
container_issue 11
container_start_page 604
publishDate 2009
institution Swansea University
issn 1759-5029
1759-5037
doi_str_mv 10.1038/nrendo.2009.195
college_str Faculty of Medicine, Health and Life Sciences
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hierarchy_top_id facultyofmedicinehealthandlifesciences
hierarchy_top_title Faculty of Medicine, Health and Life Sciences
hierarchy_parent_id facultyofmedicinehealthandlifesciences
hierarchy_parent_title Faculty of Medicine, Health and Life Sciences
department_str Swansea University Medical School - Medicine{{{_:::_}}}Faculty of Medicine, Health and Life Sciences{{{_:::_}}}Swansea University Medical School - Medicine
url http://www.nature.com/nrendo/journal/v5/n11/full/nrendo.2009.195.html
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description The primary markers of the metabolic syndrome are central obesity, insulin resistance and hypertension. In this review, we consider the effect of changes in maternal nutrition during critical windows in fetal development on an individual's subsequent predisposition to the metabolic syndrome. The fetal origins of obesity, cardiovascular disease and insulin resistance have been investigated in a wide range of epidemiological and animal studies; these investigations highlight adaptations made by the nutritionally manipulated fetus that aim to maintain energy homeostasis to ensure survival. One consequence of such developmental plasticity may be a long term re-setting of cellular energy homeostasis, most probably via epigenetic modification of genes involved in a number of key regulatory pathways. For example, reduced maternal-fetal nutrition during early gestation to midgestation affects adipose tissue development and adiposity of the fetus by setting an increased number of adipocyte precursor cells. Importantly, clinically relevant adaptations to nutritional challenges in utero may only manifest as primary components of the metabolic syndrome if followed by a period of accelerated growth early in the postnatal period and/or if offspring become obese.
published_date 2009-11-30T03:14:06Z
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