Journal article 1307 views
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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DOI (Published version): 10.1038/nrendo.2009.195
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...
Published in: | Nature Reviews Endocrinology |
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ISSN: | 1759-5029 1759-5037 |
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2009
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URI: | https://cronfa.swan.ac.uk/Record/cronfa12192 |
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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 MEDS 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 Medical School COLLEGE CODE MEDS 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 |
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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 |
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Journal article |
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Nature Reviews Endocrinology |
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5 |
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11 |
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604 |
publishDate |
2009 |
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Swansea University |
issn |
1759-5029 1759-5037 |
doi_str_mv |
10.1038/nrendo.2009.195 |
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Faculty of Medicine, Health and Life Sciences |
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facultyofmedicinehealthandlifesciences |
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Faculty of Medicine, Health and Life Sciences |
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Faculty of Medicine, Health and Life Sciences |
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Swansea University Medical School - Medicine{{{_:::_}}}Faculty of Medicine, Health and Life Sciences{{{_:::_}}}Swansea University Medical School - Medicine |
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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 |
2009-11-30T18:23:12Z |
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1822064999298760704 |
score |
11.048302 |