Nutriepigenomics Advances into Personalized Nutrition
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2017, Vol 1, Issue 2
Abstract
This review presents an omics systems perspective that presents an integrated approach to understanding the contribution of the genetic, epigenetic, metabolomic, and proteomic interactions under the influence of a dynamic nutritional environment. The review takes into account the application of genomic and post-genomic era methodologies being used to study the impact of inter-individual phenotypic differences and disease susceptibility to current and future generations. Every individual alive today is a combination of the heliotypes inherited from their parents, and the results of genetic-epigenetic interaction influencing the fetal epigenome during pre-natal development and post-natal life. Epigenetic marks imprinted in-utero are attributed to deficits in the maternal contribution to the fetal nutritional environment. Integral to this discussion is the concept of developmental plasticity, which presents itself as an unfolding narrative in the “developmental origins of health and disease” (DOHaD) hypothesis, and the ‘predictive adaptive response (PAR)’ concept. When taken together, these concepts present the case for an adaptive response to developmental programming that canpredispose an individual to future diseaseor confers an advantage. Nutriepgenomics is the study of how nutrients affect human health through epigenetic modifications. Recent advances investigating how the nutritional environment during embryonic development influences the establishment of metabolic phenotypes that can contribute to the emergence of disease are discussed. Several encouraging trials suggest that prevention and therapy of age- and lifestyle-related diseases by individualized tailoring to optimal epigenetic diets including combinations of natural products, polyphenols or drugs are conceivable. The nutritional environment influences every stage of life. Beginning with its influence on the genetic architecture of haploid cells that participate in the creation of a new individual and continues to influence processes responsible for fetal development, cellular respiration, apoptosis, and predisposition to metabolic disease. The epigenome provides an interface between the environment and the genome [1]. Epigenetic markers are enzyme-mediated chemical modifications of DNA and of its associated chromatin proteins. These modifications play key roles in regulating genomic functions, without altering the primary DNA sequence, and are transmitted with high fidelity over many cell generations. The main epigenetic mechanisms are DNA methylation, histone modifications and microRNA, which are involved in the propagation of the chromatic structure and genome activity states [2]. Discussion: Epigenetic Modifications Influence Gene Expression and Sets the Stage for Inherited Predisposition Epigenetic modifications such as DNA methylation play a key role in gene regulation and disease susceptibility.DNA methylation is an epigenetic process implicated in human disease that involves methylation of cytosine, usually at cytosine-(phosphate)-guanine (CpG) dinucleotides in the promoter region or within genes. This molecular phenotype plays a pivotal role in gene expression by affecting chromatin structure and altering the availability of coding regions to transcription mechanisms [3]. In differentiated mammalian cells, DNA methylation occurs primarily at cytosines in CG dinucleotides, so called CpG methylation, which is associated with regulation of cell specific gene expression. In contrast to DNA sequence variation, epigenetic variation is sensitive to both inherited and environmental inputs [1-3]. Patterns of DNA methylation are primarily established early in life, but may also be dynamic and change in response to environmental stimulations such as diet and exercise. DNA methylation at specific loci can be influenced by sequence variations, such that individual genotypes at a given locus may result in different patterns of DNA methylation due to allele-specific methylation. These sites are called methylation quantitative trait loci (mQTLs) and can influence the methylation pattern across an extended genomic region. A distinguishing feature of mQTLs is that they are detected across ancestry, developmental stage and tissue type [4]. Concurrently, once epigenetic modifications are introduced they can be stable and inherited, making epigenetics a potentially important pathogenic mechanism in complex metabolic diseases [1-3]. The Impact of Haplotype-dependent Allele-Specific Methylation (hap-ASM) on Disease Susceptibility A haplotype is a group of genes within an organism that was inherited together from a single parent. In addition, the term “haplotype” can also refer to the inheritance of a cluster of single nucleotide polymorphisms (SNPs), which are variations at single positions in the DNA sequence among individuals. The concept of inheritance is especially important to understanding how the nutritional environments of the parents can influence the epigenome of future generations. Haplotype-dependent allelespecific methylations (hap-ASM) can impact disease susceptibility, however maps of this phenomenon using stringent criteria in disease-relevant tissues are few in number [5]. In order to understand how hap-ASM contributes to disease, a short review is needed.
Authors and Affiliations
Joseph Curtis
Keywords
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- EP ID EP567020
- DOI 10.26717/BJSTR.2017.01.000173
- Views 139
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