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Fetal and neonatal programming of postnatal growth and feed efficiency in swine

Maternal undernutrition or overnutrition during pregnancy alters organ structure, impairs prenatal and neonatal growth and development, and reduces feed efficiency for lean tissue gains in pigs. These adverse effects may be carried over to the next generation or beyond. This phenomenon of the transg...

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Autores principales: Ji, Yun, Wu, Zhenlong, Dai, Zhaolai, Wang, Xiaolong, Li, Ju, Wang, Binggen, Wu, Guoyao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5420136/
https://www.ncbi.nlm.nih.gov/pubmed/28484595
http://dx.doi.org/10.1186/s40104-017-0173-5
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author Ji, Yun
Wu, Zhenlong
Dai, Zhaolai
Wang, Xiaolong
Li, Ju
Wang, Binggen
Wu, Guoyao
author_facet Ji, Yun
Wu, Zhenlong
Dai, Zhaolai
Wang, Xiaolong
Li, Ju
Wang, Binggen
Wu, Guoyao
author_sort Ji, Yun
collection PubMed
description Maternal undernutrition or overnutrition during pregnancy alters organ structure, impairs prenatal and neonatal growth and development, and reduces feed efficiency for lean tissue gains in pigs. These adverse effects may be carried over to the next generation or beyond. This phenomenon of the transgenerational impacts is known as fetal programming, which is mediated by stable and heritable alterations of gene expression through covalent modifications of DNA and histones without changes in DNA sequences (namely, epigenetics). The mechanisms responsible for the epigenetic regulation of protein expression and functions include chromatin remodeling; DNA methylation (occurring at the 5´-position of cytosine residues within CpG dinucleotides); and histone modifications (acetylation, methylation, phosphorylation, and ubiquitination). Like maternal malnutrition, undernutrition during the neonatal period also reduces growth performance and feed efficiency (weight gain:feed intake; also known as weight-gain efficiency) in postweaning pigs by 5–10%, thereby increasing the days necessary to reach the market body-weight. Supplementing functional amino acids (e.g., arginine and glutamine) and vitamins (e.g., folate) play a key role in activating the mammalian target of rapamycin signaling and regulating the provision of methyl donors for DNA and protein methylation. Therefore, these nutrients are beneficial for the dietary treatment of metabolic disorders in offspring with intrauterine growth restriction or neonatal malnutrition. The mechanism-based strategies hold great promise for the improvement of the efficiency of pork production and the sustainability of the global swine industry.
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spelling pubmed-54201362017-05-08 Fetal and neonatal programming of postnatal growth and feed efficiency in swine Ji, Yun Wu, Zhenlong Dai, Zhaolai Wang, Xiaolong Li, Ju Wang, Binggen Wu, Guoyao J Anim Sci Biotechnol Review Maternal undernutrition or overnutrition during pregnancy alters organ structure, impairs prenatal and neonatal growth and development, and reduces feed efficiency for lean tissue gains in pigs. These adverse effects may be carried over to the next generation or beyond. This phenomenon of the transgenerational impacts is known as fetal programming, which is mediated by stable and heritable alterations of gene expression through covalent modifications of DNA and histones without changes in DNA sequences (namely, epigenetics). The mechanisms responsible for the epigenetic regulation of protein expression and functions include chromatin remodeling; DNA methylation (occurring at the 5´-position of cytosine residues within CpG dinucleotides); and histone modifications (acetylation, methylation, phosphorylation, and ubiquitination). Like maternal malnutrition, undernutrition during the neonatal period also reduces growth performance and feed efficiency (weight gain:feed intake; also known as weight-gain efficiency) in postweaning pigs by 5–10%, thereby increasing the days necessary to reach the market body-weight. Supplementing functional amino acids (e.g., arginine and glutamine) and vitamins (e.g., folate) play a key role in activating the mammalian target of rapamycin signaling and regulating the provision of methyl donors for DNA and protein methylation. Therefore, these nutrients are beneficial for the dietary treatment of metabolic disorders in offspring with intrauterine growth restriction or neonatal malnutrition. The mechanism-based strategies hold great promise for the improvement of the efficiency of pork production and the sustainability of the global swine industry. BioMed Central 2017-05-05 /pmc/articles/PMC5420136/ /pubmed/28484595 http://dx.doi.org/10.1186/s40104-017-0173-5 Text en © The Author(s). 2017 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
Ji, Yun
Wu, Zhenlong
Dai, Zhaolai
Wang, Xiaolong
Li, Ju
Wang, Binggen
Wu, Guoyao
Fetal and neonatal programming of postnatal growth and feed efficiency in swine
title Fetal and neonatal programming of postnatal growth and feed efficiency in swine
title_full Fetal and neonatal programming of postnatal growth and feed efficiency in swine
title_fullStr Fetal and neonatal programming of postnatal growth and feed efficiency in swine
title_full_unstemmed Fetal and neonatal programming of postnatal growth and feed efficiency in swine
title_short Fetal and neonatal programming of postnatal growth and feed efficiency in swine
title_sort fetal and neonatal programming of postnatal growth and feed efficiency in swine
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5420136/
https://www.ncbi.nlm.nih.gov/pubmed/28484595
http://dx.doi.org/10.1186/s40104-017-0173-5
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