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Epigenetic Biomarkers in Nutrigenomics and Metabolism

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A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrigenetics and Nutrigenomics".

Deadline for manuscript submissions: closed (15 February 2024) | Viewed by 16242

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Special Issue Editors

Dr. Fermín Milagro

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Collection Editor

1. Center for Nutrition Research, University of Navarra, 31008 Pamplona, Spain
2. Centro de Investigación Biomédica en Red de la Fisiopatología de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III, 28029 Madrid, Spain
Interests: gene-diet
Special Issues, Collections and Topics in MDPI journals

Dr. Omar Ramos-Lopez

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Collection Editor

Medicine and Psychology School, Autonomous University of Baja California, Tijuana 22390, Mexico
Interests: nutrition; obesity; diet; chronic diseases; genetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is well known that environment–host–microbe interactions (which include nutritional status) can affect epigenetic mechanisms and shape human metabolism through long-term regulation of gene expression. This is particularly crucial in the first 1000 days of life. Additionally, growing scientific evidence supports that epigenetic signatures may affect nutrient metabolism and, consequently, health status. Accordingly, the onset and progression of metabolic diseases such as obesity, type 2 diabetes, metabolic syndrome, fatty liver disease, and cardiovascular disorders may involve epigenetic mechanisms. These include DNA methylation marks, covalent and non-covalent histone modifications, microRNA/non-coding RNA expression (in circulation or in tissues), telomere length, and imprinting phenomena. In this context, genomic, metagenomic, and nutrigenomic studies are allowing the identification of epigenetic biomarkers for predictive purposes and the design of innovative intervention strategies for disease prevention or monitoring by targeting the epigenome. Therefore, Nutrients welcomes the submission of manuscripts, either describing original research or reviewing scientific literature, on the topic of “Epigenetic Biomarkers in Nutrigenomics and Metabolism”, which highlight recent advances in the discipline for the prevention, management, and prognosis of metabolic diseases under a precision nutrition scope.

Dr. Fermín Milagro
Dr. Omar Ramos-Lopez
Collection Editors

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Keywords

DNA methylation
histone modifications
miRNA/non-coding RNA
imprinting
nutrigenomics
epigenetics
metabolic diseases

Published Papers (5 papers)

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Research

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18 pages, 2980 KiB

Open AccessArticle

The Epigenetic Legacy of Maternal Protein Restriction: Renal Ptger1 DNA Methylation Changes in Hypertensive Rat Offspring

by Huijuan Jia, Moe Miyoshi, Xuguang Li, Kyohei Furukawa, Lila Otani, Katsuhiko Shirahige, Fumihito Miura, Takashi Ito and Hisanori Kato

Nutrients 2023, 15(18), 3957; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15183957 - 13 Sep 2023

Cited by 1 | Viewed by 1034

Abstract

Nutrient imbalances during gestation are a risk factor for hypertension in offspring. Although the effects of prenatal nutritional deficiency on the development of hypertension and cardiovascular diseases in adulthood have been extensively documented, its underlying mechanisms remain poorly understood. In this study, we aimed to elucidate the precise role and functional significance of epigenetic modifications in the pathogenesis of hypertension. To this end, we integrated methylome and transcriptome data to identify potential salt-sensitive hypertension genes using the kidneys of stroke-prone spontaneously hypertensive rat (SHRSP) pups exposed to a low-protein diet throughout their fetal life. Maternal protein restriction during gestation led to a positive correlation between DNA hypermethylation of the renal prostaglandin E receptor 1 (Ptger1) CpG island and high mRNA expression of Ptger1 in offspring, which is consistently conserved. Furthermore, post-weaning low-protein or high-protein diets modified the Ptger1 DNA hypermethylation caused by fetal malnutrition. Here, we show that this epigenetic variation in Ptger1 is linked to disease susceptibility established during fetal stages and could be reprogrammed by manipulating the postnatal diet. Thus, our findings clarify the developmental origins connecting the maternal nutritional environment and potential epigenetic biomarkers for offspring hypertension. These findings shed light on hypertension prevention and prospective therapeutic strategies. Full article

(This article belongs to the Special Issue Epigenetic Biomarkers in Nutrigenomics and Metabolism)

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14 pages, 1499 KiB

Open AccessArticle

Crosstalk between Gut Microbiota and Epigenetic Markers in Obesity Development: Relationship between Ruminococcus, BMI, and MACROD2/SEL1L2 Methylation

by Francisca Salas-Perez, Taís Silveira Assmann, Omar Ramos-Lopez, J. Alfredo Martínez, Jose Ignacio Riezu-Boj and Fermín I. Milagro

Nutrients 2023, 15(7), 1550; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15071550 - 23 Mar 2023

Cited by 5 | Viewed by 1766

Abstract

Changes in gut microbiota composition and in epigenetic mechanisms have been proposed to play important roles in energy homeostasis, and the onset and development of obesity. However, the crosstalk between epigenetic markers and the gut microbiome in obesity remains unclear. The main objective of this study was to establish a link between the gut microbiota and DNA methylation patterns in subjects with obesity by identifying differentially methylated DNA regions (DMRs) that could be potentially regulated by the gut microbiota. DNA methylation and bacterial DNA sequencing analysis were performed on 342 subjects with a BMI between 18 and 40 kg/m². DNA methylation analyses identified a total of 2648 DMRs associated with BMI, while ten bacterial genera were associated with BMI. Interestingly, only the abundance of Ruminococcus was associated with one BMI-related DMR, which is located between the MACROD2/SEL1L2 genes. The Ruminococcus abundance negatively correlated with BMI, while the hypermethylated DMR was associated with reduced MACROD2 protein levels in serum. Additionally, the mediation test showed that 19% of the effect of Ruminococcus abundance on BMI is mediated by the methylation of the MACROD2/SEL1L2 DMR. These findings support the hypothesis that a crosstalk between gut microbiota and epigenetic markers may be contributing to obesity development. Full article

(This article belongs to the Special Issue Epigenetic Biomarkers in Nutrigenomics and Metabolism)

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10 pages, 274 KiB

Open AccessArticle

Mendelian Randomization Analysis of the Association of SOCS3 Methylation with Abdominal Obesity

by Yuqian Li, Xiaotian Liu, Runqi Tu, Jian Hou and Guihua Zhuang

Nutrients 2022, 14(18), 3824; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14183824 - 16 Sep 2022

Cited by 1 | Viewed by 1840

Abstract

This study was conducted to evaluate the potential causality association of SOCS3 methylation with abdominal obesity using Mendelian randomization. A case–control study, including 1064 participants, was carried out on Chinese subjects aged 18 to 79. MethylTargetTM was used to detect the methylation level for each CpG site of SOCS3, and SNPscan^® was applied to measure the single-nucleotide polymorphism (SNP) genotyping. The logistic regression was used to assess the relationship of SOCS3 methylation level and SNP genotyping with abdominal obesity. Three types of Mendelian randomization methods were implemented to examine the potential causality between SOCS3 methylation and obesity based on the SNP of SOCS3 as instrumental variables. SOCS3 methylation levels were inversely associated with abdominal obesity in five CpG sites (effect estimates ranged from 0.786 (Chr17:76356054) to 0.851 (Chr17:76356084)), and demonstrated positively association in 18 CpG sites (effect estimates ranged from 1.243 (Chr17:76354990) to 1.325 (Chr17:76355061)). The causal relationship between SOCS3 methylation and abdominal obesity was found using the maximum-likelihood method and Mendelian randomization method of penalized inverse variance weighted (MR-IVW), and the β values (95% CI) were 5.342 (0.215, 10.469) and 4.911 (0.259, 9.564), respectively. The causality was found between the SOCS3 methylation level and abdominal obesity in the Chinese population. Full article

(This article belongs to the Special Issue Epigenetic Biomarkers in Nutrigenomics and Metabolism)

14 pages, 2873 KiB

Open AccessArticle

Vitamin B12 Regulates the Transcriptional, Metabolic, and Epigenetic Programing in Human Ileal Epithelial Cells

by Yong Ge, Mojgan Zadeh and Mansour Mohamadzadeh

Nutrients 2022, 14(14), 2825; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14142825 - 09 Jul 2022

Cited by 17 | Viewed by 6921

Abstract

Vitamin B12 (VB12) is a micronutrient that is essential for DNA synthesis and cellular energy production. We recently demonstrated that VB12 oral supplementation coordinates ileal epithelial cells (iECs) and gut microbiota functions to resist pathogen colonization in mice, but it remains unclear whether VB12 directly modulates the cellular homeostasis of iECs derived from humans. Here, we integrated transcriptomic, metabolomic, and epigenomic analyses to identify VB12-dependent molecular and metabolic pathways in human iEC microtissue cultures. RNA sequencing (RNA-seq) revealed that VB12 notably activated genes involved in fatty acid metabolism and epithelial cell proliferation while suppressing inflammatory responses in human iECs. Untargeted metabolite profiling demonstrated that VB12 facilitated the biosynthesis of amino acids and methyl groups, particularly S-adenosylmethionine (SAM), and supported the function of the mitochondrial carnitine shuttle and TCA cycle. Further, genome-wide DNA methylation analysis illuminated a critical role of VB12 in sustaining cellular methylation programs, leading to differential CpG methylation of genes associated with intestinal barrier function and cell proliferation. Together, these findings suggest an essential involvement of VB12 in directing the fatty acid and mitochondrial metabolisms and reconfiguring the epigenome of human iECs to potentially support cellular oxygen utilization and cell proliferation. Full article

(This article belongs to the Special Issue Epigenetic Biomarkers in Nutrigenomics and Metabolism)

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Review

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12 pages, 690 KiB

Open AccessReview

Holistic Integration of Omics Tools for Precision Nutrition in Health and Disease

by Omar Ramos-Lopez, J. Alfredo Martinez and Fermin I. Milagro

Nutrients 2022, 14(19), 4074; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14194074 - 30 Sep 2022

Cited by 9 | Viewed by 3700

Abstract

The combination of multiple omics approaches has emerged as an innovative holistic scope to provide a more comprehensive view of the molecular and physiological events underlying human diseases (including obesity, dyslipidemias, fatty liver, insulin resistance, and inflammation), as well as for elucidating unique and specific metabolic phenotypes. These omics technologies include genomics (polymorphisms and other structural genetic variants), epigenomics (DNA methylation, histone modifications, long non-coding RNA, telomere length), metagenomics (gut microbiota composition, enterotypes), transcriptomics (RNA expression patterns), proteomics (protein quantities), and metabolomics (metabolite profiles), as well as interactions with dietary/nutritional factors. Although more evidence is still necessary, it is expected that the incorporation of integrative omics could be useful not only for risk prediction and early diagnosis but also for guiding tailored dietary treatments and prognosis schemes. Some challenges include ethical and regulatory issues, the lack of robust and reproducible results due to methodological aspects, the high cost of omics methodologies, and high-dimensional data analyses and interpretation. In this review, we provide examples of system biology studies using multi-omics methodologies to unravel novel insights into the mechanisms and pathways connecting the genotype to clinically relevant traits and therapy outcomes for precision nutrition applications in health and disease. Full article

(This article belongs to the Special Issue Epigenetic Biomarkers in Nutrigenomics and Metabolism)

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