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Nutrition, epigenetics, and developmental plasticity: implications for understanding human disease

Nutrition, epigenetics, and developmental plasticity: implications for understanding human disease
Nutrition, epigenetics, and developmental plasticity: implications for understanding human disease
There is considerable evidence for induction of differential risk of noncommunicable diseases in human by variation in the quality of the early life environment. Studies in animal models show that induction and
stability of induced changes in the phenotype of the offspring involve altered epigenetic regulation by DNAmethylation and covalentmodifications of histones. These findings indicate that such epigenetic changes are highly gene specific and function at the level of individualCpGdinucleotides.

Interventions using supplementation with folic acid ormethyl donors during pregnancy, or folic acid after weaning, alter the phenotype and epigenotype induced by maternal dietary constraint during gestation. This suggests a possible means for reducing risk of induced noncommunicable disease, although the design and conduct of such interventions may require caution. The purpose of this review is to discuss recent advances in understanding the mechanism that underlies the early life origins of disease and to place these studies in a broader life-course context.
DNA methylation, fetal development, cardio-metabolic disease, folate
0199-9885
Burdge, Graham C.
09d60a07-8ca1-4351-9bf1-de6ffcfb2159
Lillycrop, Karen A.
eeaaa78d-0c4d-4033-a178-60ce7345a2cc
Burdge, Graham C.
09d60a07-8ca1-4351-9bf1-de6ffcfb2159
Lillycrop, Karen A.
eeaaa78d-0c4d-4033-a178-60ce7345a2cc

Burdge, Graham C. and Lillycrop, Karen A. (2010) Nutrition, epigenetics, and developmental plasticity: implications for understanding human disease. Annual Review of Nutrition, 30. (doi:10.1146/annurev.nutr.012809.104751). (In Press)

Record type: Article

Abstract

There is considerable evidence for induction of differential risk of noncommunicable diseases in human by variation in the quality of the early life environment. Studies in animal models show that induction and
stability of induced changes in the phenotype of the offspring involve altered epigenetic regulation by DNAmethylation and covalentmodifications of histones. These findings indicate that such epigenetic changes are highly gene specific and function at the level of individualCpGdinucleotides.

Interventions using supplementation with folic acid ormethyl donors during pregnancy, or folic acid after weaning, alter the phenotype and epigenotype induced by maternal dietary constraint during gestation. This suggests a possible means for reducing risk of induced noncommunicable disease, although the design and conduct of such interventions may require caution. The purpose of this review is to discuss recent advances in understanding the mechanism that underlies the early life origins of disease and to place these studies in a broader life-course context.

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More information

Accepted/In Press date: August 2010
Keywords: DNA methylation, fetal development, cardio-metabolic disease, folate

Identifiers

Local EPrints ID: 144917
URI: https://eprints.soton.ac.uk/id/eprint/144917
ISSN: 0199-9885
PURE UUID: 8b493b77-addc-4024-a7e4-ae0da423512c
ORCID for Graham C. Burdge: ORCID iD orcid.org/0000-0002-7665-2967
ORCID for Karen A. Lillycrop: ORCID iD orcid.org/0000-0001-7350-5489

Catalogue record

Date deposited: 20 May 2010 09:09
Last modified: 06 Jun 2018 13:11

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