The Effect of Nutrition during Early Life on the Epigenetic Regulation of Transcription and Implications for Human DiseasesLillycrop K.A.a · Burdge G.C.b
aCentre for Biological Sciences, Institute of Developmental Sciences, Faculty of Natural and Environmental Sciences, and bAcademic Unit of Human Development and Health, Institute of Developmental Sciences, Faculty of Medicine, University of Southampton, Southampton, UK
Epigenetic processes which include DNA methylation, histone modification and miRNAs are integral in determining when and where specific genes are expressed. There is now increasing evidence that the epigenome is susceptible to a variety of environmental cues, such as nutrition, during specific periods of development. The changes induced by early-life nutrition may reflect an adaptive response of the foetus to environmental cues acting through the process of developmental plasticity. This may allow an organism to adjust its developmental programme resulting in long-term changes in its metabolism and physiology in order to be better matched to the future environment. However, when the future environment lies outside the anticipated range, metabolic and homoeostatic capacity will be mismatched with the environment and that individual will be at increased risk of developing a range of non-communicable diseases. Thus the environmental regulation of epigenetic processes is a central component in the developmental origins of non-communicable diseases and our understanding of these processes is, therefore, critical both for the identification of individuals at risk and for the development of new intervention strategies.
© 2012 S. Karger AG, Basel
Abbreviations: Avy = Agouti viable yellow; CVD = cardiovascular disease; CpG = cytosine and guanine nucleotides linked by phosphate; Dnmt = DNA methyltransferase; GR = glucocorticoid receptor; IGF = insulin growth factor; MeCP = methyl CpG binding protein; miRNA = microRNA; Pdx1 = pancreatic and duodenal homeobox 1; POMC = Pro-opiomelanocortin; PR = protein restricted; PPAR = peroxisomal proliferator-activated receptor.
Published online: February 22, 2012
Number of Print Pages : 13
Number of Figures : 2, Number of Tables : 0, Number of References : 84
Journal of Nutrigenetics and Nutrigenomics
Vol. 4, No. 5, Year 2011 (Cover Date: February 2012)
Journal Editor: Pérusse L. (Quebec, Que.)
ISSN: 1661-6499 (Print), eISSN: 1661-6758 (Online)
For additional information: http://www.karger.com/JNN