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Nutriepigenomics
Nutriepigenomics is the study of food nutrients and their effects on human health through epigenetic modifications. There is now considerable evidence that nutritional imbalances during gestation and lactation are linked to non-communicable diseases, such as obesity, cardiovascular disease, diabetes, hypertension, and cancer. If metabolic disturbances occur during critical time windows of development, the resulting epigenetic alterations can lead to permanent changes in tissue and organ structure or function and predispose individuals to disease.〔Gallou-Kabani C, Vige A, Gross MS, Junien C. Nutri-epigenomics: Lifelong remodelling of our epigenomes by nutritional and metabolic factors and beyond. Clin Chem Lab Med. 2007;45(3):321-7 PMID 17378726〕
== Overview ==
Epigenetics relates to heritable changes in gene function that occur independently of alterations in primary DNA sequence. Two major epigenetic mechanisms implicated in nutriepigenomics are DNA methylation and histone modification. DNA methylation in gene promoter regions usually results in gene silencing and influences gene expression. While this form of gene silencing is extremely important in development and cellular differentiation, aberrant DNA methylation can be detrimental and has been linked to various disease processes, such as cancer.〔Berdasco M, Esteller M. Aberrant epigenetic landscape in cancer: How cellular identity goes awry. Dev Cell. 2010 Nov 16;19(5):698-711 PMID 21074720.〕 The methyl groups used in DNA methylation are often derived from dietary sources, such as folate and choline, and explains why diet can have a significant impact on methylation patterns and gene expression.〔Pozharny Y, Lambertini L, Clunie G, Ferrara L, Lee MJ. Epigenetics in women's health care. Mt Sinai J Med. 2010 Mar;77(2):225-35 PMID 20309920.〕 Gene silencing can also be reinforced through the recruitment of histone deacetylases to decrease transcriptional activation. Conversely, histone acetylation induces transcriptional activation to increase gene expression. Dietary components can influence these epigenetic events, thereby altering gene expression and disturbing functions such as appetite control, metabolic balance and fuel utilization.〔Gallou-Kabani C, Vige A, Gross MS, Junien C. Nutri-epigenomics: Lifelong remodelling of our epigenomes by nutritional and metabolic factors and beyond. Clin Chem Lab Med. 2007;45(3):321-7〕
Various genetic sequences can be targeted for epigenetic modification. A transcriptome-wide analysis in mice found that a protein-restricted (PR) diet during gestation resulted in differential gene expression in approximately 1% of the fetal genes analyzed (235/22,690). Specifically, increased expression was seen in genes involved in the p53 pathway, apoptosis, negative regulators of cell metabolism, and genes related to epigenetic control.〔Gheorghe CP, Goyal R, Holweger JD, Longo LD. Placental gene expression responses to maternal protein restriction in the mouse. Placenta. 2009 May;30(5):411-7 PMID 19362366〕 Additional studies have investigated the effect of a PR-diet in rats and found changes in promoter methylation of both the glucocorticoid receptor and peroxisome proliferator-activated receptor (PPAR).〔Lillycrop KA, Phillips ES, Torrens C, Hanson MA, Jackson AA, Burdge GC. Feeding pregnant rats a protein-restricted diet persistently alters the methylation of specific cytosines in the hepatic PPAR alpha promoter of the offspring. Br J Nutr. 2008 Aug;100(2):278-82 PMID 18186951〕〔Lillycrop KA, Slater-Jefferies JL, Hanson MA, Godfrey KM, Jackson AA, Burdge GC. Induction of altered epigenetic regulation of the hepatic glucocorticoid receptor in the offspring of rats fed a protein-restricted diet during pregnancy suggests that reduced DNA methyltransferase-1 expression is involved in impaired DNA methylation and changes in histone modifications. Br J Nutr. 2007 Jun;97(6):1064-73 PMID 17433129〕 Altered expression of these receptors can result in elevated blood glucose levels and affect lipid and carbohydrate metabolism.〔Pozharny Y, Lambertini L, Clunie G, Ferrara L, Lee MJ. Epigenetics in women's health care. Mt Sinai J Med. 2010 Mar;77(2):225-35 PMID 20309920〕 Feeding a PR-diet to pregnant and/or lactating mice also increased expression of glucokinase, acetyl-CoA carboxylase, PPARα, and acyl-CoA oxidase.〔Burdge GC, Lillycrop KA. Nutrition, epigenetics, and developmental plasticity: Implications for understanding human disease. Annu Rev Nutr. 2010 Aug 21;30:315-39 PMID 20415585〕 Changes in expression were reportedly due to epigenetic regulation of either the gene promoter itself, or promoters of transcription factors that regulate gene expression. Additional genes that have been shown, either by in vitro or in vivo studies, to be regulated by epigenetic mechanisms include leptin, SOCS3, glucose transporter (GLUT)-4, POMC, 11-β-hydroxysteroid dehydrogenase type 2 and corticotrophin releasing hormone. Epigenetic modification of these genes may lead to “metabolic programming” of the fetus and result in long-term changes in metabolism and energy homeostasis.〔Tamashiro KL, Moran TH. Perinatal environment and its influences on metabolic programming of offspring. Physiol Behav. 2010 Jul 14;100(5):560-6 PMID 20394764〕
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