Early nutrition, epigenetic changes at transposons and imprinted genes, and enhanced susceptibility to adult chronic diseases

Abstract

Several recent reviews surveying the promising field of nutrigenomics1,2 have not discussed the important role that epigenetic mechanisms play at the nexus between nutrition and the genome. This is a glaring omission. Certainly, “nutrient–gene interactions” in humans enable various nutrients to transiently influence the expression of specific subsets of genes. In addition to these phenomena, however, it is becoming increasingly evident that by interacting with epigenetic mechanisms, which regulate chromatin conformation across entire genomic regions, transient nutritional stimuli at critical ontogenic stages can wield lasting influences on the expression of various genes.3 Moreover, such epigenetic changes, if they occur in the gametes, may be heritable. This review focuses on early nutritional influences on cytosine methylation. It proposes that certain genomic regions, including genomically imprinted domains and specific transposon insertion sites, are especially labile to such influences. Considering the critical roles that genomically imprinted genes play in mammalian growth and development4 and the huge proportion of our genome that is comprised of transposons,5 early nutritional influences on these genomic components could have a substantial impact on human health. Genomic and epigenetic similarities between these distinct classes of elements are elaborated, and key areas of future research are discussed.