Impact of Maternal Diet on the Epigenome during In Utero Life and the Developmental Programming of Diseases in Childhood and Adulthood

• Published in: Nutrients 2015-11, Vol.7 (11), p.9492-9507
• Main Author: Lee, Ho-Sun
• Format: Article
• Language: English
• Subjects: Animals; Cardiovascular Diseases - genetics; development; Diabetes Mellitus, Type 2 - genetics; Diet; Disease Models, Animal; DNA Methylation; Epigenesis, Genetic; epigenetics; Epigenomics; Female; Gene-Environment Interaction; Humans; maternal nutrients; Maternal Nutritional Physiological Phenomena; metabolic syndrome; Nutritional Status; Phenotype; Pregnancy; Prenatal Exposure Delayed Effects; Review
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu7115467

Exposure to environmental factors in early life can influence developmental processes and long-term health in humans. Early life nutrition and maternal diet are well-known examples of conditions shown to influence the risk of developing metabolic diseases, including type 2 diabetes mellitus and cardiovascular diseases, in adulthood. It is increasingly accepted that environmental compounds, including nutrients, can produce changes in the genome activity that, in spite of not altering the DNA sequence, can produce important, stable and, in some instances, transgenerational alterations in the phenotype. Epigenetics refers to changes in gene function that cannot be explained by changes in the DNA sequence, with DNA methylation patterns/histone modifications that can make important contributions to epigenetic memory. The epigenome can be considered as an interface between the genome and the environment that is central to the generation of phenotypes and their stability throughout the life course. To better understand the role of maternal health and nutrition in the initiation and progression of diseases in childhood and adulthood, it is necessary to identify the physiological and/or pathological roles of specific nutrients on the epigenome and how dietary interventions in utero and early life could modulate disease risk through epigenomic alteration.