Prenatal nutrition and the risk of adult obesity: Long-term effects of nutrition on epigenetic mechanisms regulating gene expression

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• dc.contributor.author Navarro, Estanislauca
• dc.contributor.author Funtikova, Anna N.ca
• dc.contributor.author Fitó Colomer, Montserratca
• dc.contributor.author Schröder, Helmut, 1958-ca
• dc.date.accessioned 2017-06-26T10:09:36Z
• dc.date.issued 2017
• dc.description.abstract Solid epidemiological evidence indicates that part of the risk of obesity in adulthood could be programmed during prenatal development by the quality of maternal nutrition. Nevertheless, the molecular mechanisms involved are mostly unknown, which hinders our capacity to develop effective intervention policies. Here, we discuss the hypothesis that mechanisms underlying prenatal programming of adult risk are epigenetic and sensitive to environmental cues such as nutrition. While the information encoded in DNA is essentially stable, regulatory epigenetic mechanisms include reversible, covalent modifications of DNA and chromatin, such as methylation, acetylation etc. It is known that dietary availability of methyl donors has an impact on the patterns of gene expression by affecting DNA methylation at regulatory regions, a likely basis for reprogramming developmental plasticity. The Agouti and Axin-fused genes, as well as the embryonic growth factor IGF2/H19 locus are examples of diet-induced modulation of phenotypic traits by affecting methylation of gene-regulatory regions. Recent work has evidenced an unsuspected role for chromatin as metabolic sensor. Chromatin is susceptible to a number of post-translational modifications that modulate gene expression, among them the GlcNAcylation of histone proteins and other epigenetic regulators. Intracellular levels of the precursor molecule UDP-GlcNAc, and hence the degree of global chromatin GlcNAcylation, depend on the energetic state of the cell, making GlcNAcylation a functional link between nutrition and regulation of gene expression. Dietary interference with these regulatory mechanisms could effectively counteract the early-life programming of adult risk.
• dc.description.sponsorship This research was supported by a grant (2FD097-0297-CO2-01) from Fondo Europeo de Desarrollo Regional (FEDER); by a scholarship for PhD training from a national program to prepare university professors (FPU), Ministry of Education of Spain (AP2010-3198); and also partially supported by FEDER [CB06/02/0029] and Red Investigación Cardiovascular, HERACLES [RD12/0042]), and AGAUR (2014 SGR 240) and (2014 SGR 0334). The CIBERESP and CIBEROBN are initiatives of the Instituto de Salud Carlos III, Madrid, Spain
• dc.format.mimetype application/pdfca
• dc.identifier.citation Navarro E, Funtikova AN, Fíto M, Schröder H. Prenatal nutrition and the risk of adult obesity: Long-term effects of nutrition on epigenetic mechanisms regulating gene expression. J Nutr Biochem. 2017 Jan; 39: 1-14. DOI: 10.1016/j.jnutbio.2016.03.012
• dc.identifier.doi http://dx.doi.org/10.1016/j.jnutbio.2016.03.012
• dc.identifier.issn 0955-2863
• dc.identifier.uri http://hdl.handle.net/10230/32465
• dc.language.iso eng
• dc.publisher Elsevierca
• dc.relation.ispartof Journal of Nutritional Biochemistry. 2017 Jan;39:1-14
• dc.relation.projectID info:eu-repo/grantAgreement/ES/3PN/AP2010-3198
• dc.rights © Elsevier http://dx.doi.org/10.1016/j.jnutbio.2016.03.012
• dc.rights.accessRights info:eu-repo/semantics/openAccess
• dc.subject.other Embaràs -- Aspectes nutricionals
• dc.subject.other Obesitat
• dc.subject.other Epigenètica
• dc.subject.other Expressió gènica
• dc.title Prenatal nutrition and the risk of adult obesity: Long-term effects of nutrition on epigenetic mechanisms regulating gene expressionca
• dc.type info:eu-repo/semantics/article
• dc.type.version info:eu-repo/semantics/acceptedVersion