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Epigenetic mechanisms for nutrition determinants of later health outcomes^1,2,3,4

¹ From the Nutrition Research Institute, the University of North Carolina, Chapel Hill, NC.

² Presented at the workshop "Early Risk Determinants and Later Health Outcomes: Implications for Research Prioritization and the Food Supply," held in Washington, DC, July 8–9, 2008.

³ Supported by grants from the National Institutes of Health (DK55865, AG09525) to the author and to the UNC Clinical Nutrition Research Unit (DK56350). Funds to support the writing of this manuscript were provided in part by the Project Committee on Early Nutrition of the International Life Sciences Institute North American Branch.

⁴ Address requests for reprints and correspondence to SH Zeisel, Nutrition Research Institute, Department of Nutrition, School of Public Health and School of Medicine, University of North Carolina, CB# 7461, Chapel Hill, NC 27599. E-mail: steven_zeisel{at}unc.edu.

ABSTRACT

Epigenetic marking on genes can determine whether or not genes are expressed. Epigenetic regulation is mediated by the addition of methyl groups to DNA cytosine bases, of methyl and acetyl groups to proteins (histones) around which DNA is wrapped, and by small interfering RNA molecules. Some components of epigenetic regulation have evolved to permit control of whether maternal or paternal genes are expressed. The epigenetic imprinting of IGF2 expression is an example of maternal and paternal epigenetic marking that modulates fetal growth and fetal size. However, epigenetic regulation also permits the fetus and the infant to adapt gene expression to the environment in which it is growing; sometimes when this adjustment goes awry, the risk of chronic disease is increased. Recent progress in the understanding of nutritional influences on epigenetics suggests that nutrients that are part of methyl-group metabolism can significantly influence epigenetics. During critical periods in development, dietary methyl-group intake (choline, methionine, and folate) can alter DNA and histone methylation, which results in lifelong changes in gene expression. In rodent models, pregnant dams that were fed diets high in methionine, folic acid, and choline produced offspring with different coat colors or with kinked tails. A number of syndromes in humans can be caused by defective epigenetic regulation, including Rett syndrome. There are interesting examples of the effects of nutrition in early life that result in altered health in adults, and some of these could be the result of altered epigenetic regulation of gene expression.

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