Abstract
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.
Highlights
Maternal diet plays a critical role in fetal growth and development
Distinct programs of gene expression underlying the development of different cell lineages and tissues are executed without changes in the genome (DNA sequence)
Epigenetic reprogramming is essential during embryonic and early postnatal development, and epigenetic deregulation is recognized to play a role in the etiology of several developmental syndromes
Summary
Maternal diet plays a critical role in fetal growth and development. Pregnancy is associated with increased nutritional needs due to the physiological changes of the mother and the metabolic demands of the embryo/fetus (conceptus). A growing number of studies focusing on the developmental origin of health and disease have identified links between early nutrition and disease, consistent with the “developmental origins of health and disease” (DOHaD) hypothesis [2] This hypothesis postulates that early life development is critically sensitive to inadequate nutrition and other environmental factors, leading to permanent changes in development that can influence the health of an individual in later life and the risk of disease [2,3]. Should some of the epigenetic mechanisms underlie developmental plasticity in the DOHaD and disease-related outcomes result from disruptions of the epigenome induced by the fetal environment, this emerging field may provide critical insights into the role of early life events on disease programming in childhood and adulthood [4]. We review recent evidence on the potential of maternal diet in utero to counteract epigenetic alterations and phenotypic outcomes and discuss its implications on novel strategies for epigenetic chemoprevention during pregnancy
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