1 Department of Nutrition and Dietetics, Faculty of Pharmacy, University of Concepcion, Concepcion, Chile
2 Master Program in Human Nutrition, Faculty of Pharmacy, University of Concepcion, Concepcion, Chile
3 School of Nutrition and Dietetics, Faculty of Health, University of Talca, Talca, Chile
4 Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, University of Concepción, Concepción, Chile
The maternal environment influences embryonic and fetal life. Nutritional deficits or excesses alter the trajectory of fetus/offspring’s development. The concept of “developmental programming” and “developmental origins of health and disease” consists of the idea that maternal diet may remodel the genome and lead to epigenetic changes. These changes are induced during early life, permanently altering the phenotype in the posterior adult stage, favoring the development of metabolic diseases such as obesity, dyslipidemia, hypertension, hyperinsulinemia, and metabolic syndrome. In this review, it is aimed to overview epigenetics, maternal diet and metabolic programming factors and determine which of these might affect future generations.
Scope and Approach:
Nutrients interfere with the epigenome by influencing the supply and use of methyl groups through DNA transmethylation and demethylation mechanisms. They also influence the remodeling of chromatin and arginine or lysine residues at the N-terminal tails of histone, thus altering miRNA expression. Fats, proteins, B vitamins and folates act as important cofactors in methylation processes. The metabolism of carbon in the methyl groups of choline, folic acid and methionine to S-Adenosyl Methionine (SAM), acts as methyl donors to methyl DNA, RNA, and proteins. B-complex vitamins are important since they act as coenzymes during this process.
Key Findings and Conclusion:
Nutrients, during pregnancy, potentially influence susceptibility to diseases in adulthood. Additionally, the deficit or excess of nutrients alter the epigenetic machinery, affecting genes and influencing the genome of the offspring and therefore, predisposing the development of chronic diseases in adults.
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* Address correspondence to this author at the Department of Nutrition and Dietetics, Faculty of Pharmacy, University of Concepcion, 4070386 - Concepcion, Chile; Tel: +56 41266 1671 ; Email: firstname.lastname@example.org