DNA Methylation and Nutrition
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1
Aristotle University of Thessaloniki, Department of Pharmacology, Greece
Introduction: Nutrigenomics, the study of bidirectional interactions between genes and diet, is a rapidly developing new promising scientific area, which is promising to change future research and practice in human nutrition. There are 3 major mechanisms in nutrient – gene interactions, involving 1) direct interactions: nutrients behave as transcription factors that bind to DNA and acutely induce gene expression, 2) epigenetic interactions: nutrients can alter the DNA or histone proteins’ structure, resulting in alteration of gene expression, and 3) genetic variations: common genetic variations [single nucleotide polymorphisms (SNPs)] can alter the expression or function of genes.
Epigenetic interactions: Epigenetic regulation is mediated by the addition of methyl groups catalyzed by DNA methyltransferase to DNA cytosine bases, followed by guanosine (5΄CpG-3΄ sites) and of methyl and acetyl groups to histones, around which DNA is wrapped. In mammals, most (90–98%) CpG sites in DNA are methylated. However, specific CpG-rich areas of DNA, where most CpGs are not methylated, exist. These areas are known as CpG islands. Methylated CpG islands, when located at the promoter region, attract capping proteins that hinder access to the gene for the transcription factors that normally induce gene expression. Thus, increased methylation is usually associated with gene silencing or reduced gene expression. On the other hand, methylation and acetylation of histones can uncoil them, creating channels through which transcription factors can pass and activate gene promoters leading to gene over expression.
Methyl donors and metabolic pathways: The active methylating agent for DNA methylation is S-adenosylmethionine (SAM) the availability of which is directly influenced by diet. SAM is formed from methyl groups derived from choline and its metabolite betaine, methionine and methyl-tetrahydrofolate (methyl-THF). Transmethylation metabolic pathways closely interconnect choline, methionine, methyl-THF and vitamins B6 and B12. The pathways are related at the point at which homocysteine is converted into methionine, which via methionine adenosyltransferase is converted to SAM. Changes in the metabolism of one of these pathways results in compensatory changes to the others.
Conclusion: Diet can directly influence epigenetic marking because DNA methylation that influences the expression of genes depends upon the availability of methyl donors derived from nutrients. Some of these epigenetic marks can be inherited and play an important role in successful completion of fetal development.
Keywords:
nutrition,
Nutrigenomics,
DNA Methylation,
methyl donor
Conference:
8th Southeast European Congress on Xenobiotic Metabolism and Toxicity - XEMET 2010, Thessaloniki, Greece, 1 Oct - 5 Oct, 2010.
Presentation Type:
Poster
Topic:
Nutrigenomics
Citation:
Tsalidou
M and
Papaioannidou
P
(2010). DNA Methylation and Nutrition.
Front. Pharmacol.
Conference Abstract:
8th Southeast European Congress on Xenobiotic Metabolism and Toxicity - XEMET 2010.
doi: 10.3389/conf.fphar.2010.60.00207
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Received:
28 Oct 2010;
Published Online:
04 Nov 2010.
*
Correspondence:
Dr. Paraskevi Papaioannidou, Aristotle University of Thessaloniki, Department of Pharmacology, Thessaloniki, Greece, ppap@auth.gr