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Influence of gestational salt restriction in fetal growth and in development of diseases in adulthood
Recent studies reported the critical role of the intrauterine environment of a fetus in growth or the development of disease in adulthood. In this article we discussed the implications of salt restriction in growth of a fetus and the development of growth-related disease in adulthood. Salt restricti...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4719732/ https://www.ncbi.nlm.nih.gov/pubmed/26787358 http://dx.doi.org/10.1186/s12929-016-0233-8 |
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author | Sakuyama, Hiroe Katoh, Minami Wakabayashi, Honoka Zulli, Anthony Kruzliak, Peter Uehara, Yoshio |
author_facet | Sakuyama, Hiroe Katoh, Minami Wakabayashi, Honoka Zulli, Anthony Kruzliak, Peter Uehara, Yoshio |
author_sort | Sakuyama, Hiroe |
collection | PubMed |
description | Recent studies reported the critical role of the intrauterine environment of a fetus in growth or the development of disease in adulthood. In this article we discussed the implications of salt restriction in growth of a fetus and the development of growth-related disease in adulthood. Salt restriction causes retardation of fatal growth or intrauterine death thereby leading to low birth weight or decreased birth rate. Such retardation of growth along with the upregulation of the renin angiotensin system due to salt restriction results in the underdevelopment of cardiovascular organs or decreases the number of the nephron in the kidney and is responsible for onset of hypertension in adulthood. In addition, gestational salt restriction is associated with salt craving after weaning. Moreover, salt restriction is associated with a decrease in insulin sensitivity. A series of alterations in metabolism due to salt restriction are probably mediated by the upregulation of the renin angiotensin system and an epigenetic mechanism including proinflammatory substances or histone methylation. Part of the metabolic disease in adulthood may be programmed through such epigenetic changes. The modification of gene in a fetus may be switched on through environment factors or life style after birth. The benefits of salt restriction have been assumed thus far; however, more precise investigation is required of its influence on the health of fetuses and the onset of various diseases in adulthood. |
format | Online Article Text |
id | pubmed-4719732 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-47197322016-01-21 Influence of gestational salt restriction in fetal growth and in development of diseases in adulthood Sakuyama, Hiroe Katoh, Minami Wakabayashi, Honoka Zulli, Anthony Kruzliak, Peter Uehara, Yoshio J Biomed Sci Review Recent studies reported the critical role of the intrauterine environment of a fetus in growth or the development of disease in adulthood. In this article we discussed the implications of salt restriction in growth of a fetus and the development of growth-related disease in adulthood. Salt restriction causes retardation of fatal growth or intrauterine death thereby leading to low birth weight or decreased birth rate. Such retardation of growth along with the upregulation of the renin angiotensin system due to salt restriction results in the underdevelopment of cardiovascular organs or decreases the number of the nephron in the kidney and is responsible for onset of hypertension in adulthood. In addition, gestational salt restriction is associated with salt craving after weaning. Moreover, salt restriction is associated with a decrease in insulin sensitivity. A series of alterations in metabolism due to salt restriction are probably mediated by the upregulation of the renin angiotensin system and an epigenetic mechanism including proinflammatory substances or histone methylation. Part of the metabolic disease in adulthood may be programmed through such epigenetic changes. The modification of gene in a fetus may be switched on through environment factors or life style after birth. The benefits of salt restriction have been assumed thus far; however, more precise investigation is required of its influence on the health of fetuses and the onset of various diseases in adulthood. BioMed Central 2016-01-20 /pmc/articles/PMC4719732/ /pubmed/26787358 http://dx.doi.org/10.1186/s12929-016-0233-8 Text en © Sakuyama et al. 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Review Sakuyama, Hiroe Katoh, Minami Wakabayashi, Honoka Zulli, Anthony Kruzliak, Peter Uehara, Yoshio Influence of gestational salt restriction in fetal growth and in development of diseases in adulthood |
title | Influence of gestational salt restriction in fetal growth and in development of diseases in adulthood |
title_full | Influence of gestational salt restriction in fetal growth and in development of diseases in adulthood |
title_fullStr | Influence of gestational salt restriction in fetal growth and in development of diseases in adulthood |
title_full_unstemmed | Influence of gestational salt restriction in fetal growth and in development of diseases in adulthood |
title_short | Influence of gestational salt restriction in fetal growth and in development of diseases in adulthood |
title_sort | influence of gestational salt restriction in fetal growth and in development of diseases in adulthood |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4719732/ https://www.ncbi.nlm.nih.gov/pubmed/26787358 http://dx.doi.org/10.1186/s12929-016-0233-8 |
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