Special Issue "Nutrition and Epigenetics"

A special issue of Nutrients (ISSN 2072-6643).

Deadline for manuscript submissions: 10 December 2019.

Special Issue Editors

Prof. Dr. Giuseppe Passarino
E-Mail Website
Guest Editor
Department of Biology, Ecology and Earth Science, University of Calabria, 87036 Rende, Italy
Interests: epigenetics; genetic variability; aging; molecular health biomarkers
Prof. Dr. Alberto Montesanto
E-Mail Website
Guest Editor
Department of Biology, University of Calabria, 87036 Rende, Italy
Interests: epigenetics; aging; statistical genetics
Prof. Dr. Dina Bellizzi
E-Mail Website
Guest Editor
Department of Biology, University of Calabria, 87036 Rende, Italy
Interests: epigenetics; epigenetic biomarkers; aging

Special Issue Information

Dear Colleagues,

Epigenetics has been rapidly arising as a major topic in molecular biology and genetics. Nutrition is certainly among the most important external factors influencing the epigenetic profile. Pioneering studies have shown the importance of nutrition in modulating the fate of different organisms, such as honey bees and rodents. More recently, the long-term effects of diet on gene expression variations are increasingly recognized as major regulators that influence the phenotypic plasticity, as well as health and lifespan, via epigenetic modifications. In mammals, nutrient availability has been shown to induce epigenetic modifications at both global and locus-specific levels through a variety of molecular mechanisms, which mainly involve mitochondrial activity. More particularly, the bioavailability of S-adenosylmethionine (SAM), the substrate for the methyltransferase reactions, is regulated by the dietary intake of vitamin B2, B6, and B12. Therefore, studies carried out, mostly in rodents, revealed that a diet deficient in or supplemented with methyl donors is responsible for global DNA hypo-methylation and hyper-methylation, respectively. In addition, calorie restriction (CR), namely the reduction of food intake widely recognized to extend longevity in different species, leads to aberrant DNA methylation patterns by modulating DNMT activities.

In this Issue of Nutrients, we would like to gather papers dealing with the interaction between nutrition and epigenetic modifications, in particular, DNA methylation modifications. Our aim is to outline the state-of-the-art on this field and to bring to the attention of the readers the issues that will be the most important topics in the near future.

Prof. Giuseppe Passarino
Prof. Dr. Alberto Montesanto
Prof. Dr. Dina Bellizzi
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Nutrition
  • Dietary habits
  • Epigenetics
  • Methylation

Published Papers (3 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Open AccessArticle
mir-101-3p Downregulation Promotes Fibrogenesis by Facilitating Hepatic Stellate Cell Transdifferentiation During Insulin Resistance
Nutrients 2019, 11(11), 2597; https://doi.org/10.3390/nu11112597 - 29 Oct 2019
Abstract
Insulin resistance (IR) and microRNAs (miRNAs), which regulate cell-to-cell communication between hepatocytes and hepatic stellate cells (HSCs), may intertwine in nonalcoholic fatty liver disease (NAFLD) pathogenesis. The aim of this study was to evaluate whether epigenetics and environmental factors interact to promote progressive [...] Read more.
Insulin resistance (IR) and microRNAs (miRNAs), which regulate cell-to-cell communication between hepatocytes and hepatic stellate cells (HSCs), may intertwine in nonalcoholic fatty liver disease (NAFLD) pathogenesis. The aim of this study was to evaluate whether epigenetics and environmental factors interact to promote progressive NAFLD during IR. We examined the miRNA signature in insulin receptor haploinsufficient (InsR+/−) and wild-type (wt) HSCs by RNAseq (n = 4 per group). Then, we evaluated their impact in an IR-NASH (nonalcoholic steatohepatitis) model (InsR+/− mice fed standard or methionine choline deficient (MCD) diet, n = 10 per group) and in vitro. InsR+/− HSCs displayed 36 differentially expressed miRNAs (p < 0.05 vs. wt), whose expression was then analyzed in the liver of InsR+/− mice fed an MCD diet. We found that miR-101-3p negatively associated with both InsR+/− genotype and MCD (p < 0.05) and the histological spectrum of liver damage (p < 0.01). miR-101-3p was reduced in InsR+/− hepatocytes and HSCs and even more in InsR+/− cells exposed to insulin (0.33 µM) and fatty acids (0.25 mM), resembling the IR-NASH model. Conversely, insulin induced miR-101-3p expression in wt cells but not in InsR+/− ones (p < 0.05). In conclusion, IR combined with diet-induced liver injury favors miR-101-3p downregulation, which may promote progressive NAFLD through HSC and hepatocyte transdifferentiation and proliferation. Full article
(This article belongs to the Special Issue Nutrition and Epigenetics)
Show Figures

Figure 1

Open AccessArticle
Maternal Low-Fat Diet Programs the Hepatic Epigenome despite Exposure to an Obesogenic Postnatal Diet
Nutrients 2019, 11(9), 2075; https://doi.org/10.3390/nu11092075 - 03 Sep 2019
Abstract
Obesity and metabolic disease present a danger to long-term health outcomes. It has been hypothesized that epigenetic marks established during early life might program individuals and have either beneficial or harmful consequences later in life. In the present study, we examined whether maternal [...] Read more.
Obesity and metabolic disease present a danger to long-term health outcomes. It has been hypothesized that epigenetic marks established during early life might program individuals and have either beneficial or harmful consequences later in life. In the present study, we examined whether maternal diet alters DNA methylation and whether such modifications persist after an obesogenic postnatal dietary challenge. During gestation and lactation, male Sprague-Dawley rats were exposed to either a high-fat diet (HF; n = 10) or low-fat diet (LF; n = 10). After weaning, all animals were fed a HF diet for an additional nine weeks. There were no differences observed in food intake or body weight between groups. Hepatic DNA methylation was quantified using both methylated DNA immunoprecipitation sequencing (MeDIP-seq) and methylation-sensitive restriction enzyme sequencing (MRE-seq). Overall, 1419 differentially methylated regions (DMRs) were identified. DMRs tended to be located in CpG shores and were enriched for genes involved in metabolism and cancer. Gene expression was measured for 31 genes in these pathways. Map3k5 and Igf1r were confirmed to be differentially expressed. Finally, we attempted to quantify the functional relevance of intergenic DMRs. Using chromatin contact data, we saw that conserved DMRs were topologically associated with metabolism genes, which were associated with differential expression of Adh5, Enox1, and Pik3c3. We show that although maternal dietary fat is unable to reverse offspring weight gain in response to a postnatal obesogenic diet, early life diet does program the hepatic methylome. Epigenetic alterations occur primarily in metabolic and cancer pathways and are associated with altered gene expression, but it is unclear whether they bear consequence later in life. Full article
(This article belongs to the Special Issue Nutrition and Epigenetics)
Show Figures

Figure 1

Open AccessArticle
Network Analysis of the Potential Role of DNA Methylation in the Relationship between Plasma Carotenoids and Lipid Profile
Nutrients 2019, 11(6), 1265; https://doi.org/10.3390/nu11061265 - 04 Jun 2019
Abstract
Variability in plasma carotenoids may be attributable to several factors including genetic variants and lipid profile. Until now, the impact of DNA methylation on this variability has not been widely studied. Weighted gene correlation network analysis (WGCNA) is a systems biology method used [...] Read more.
Variability in plasma carotenoids may be attributable to several factors including genetic variants and lipid profile. Until now, the impact of DNA methylation on this variability has not been widely studied. Weighted gene correlation network analysis (WGCNA) is a systems biology method used for finding gene clusters (modules) with highly correlated methylation levels and for relating them to phenotypic traits. The objective of the present study was to examine the role of DNA methylation in the relationship between plasma total carotenoid concentrations and lipid profile using WGCNA in 48 healthy subjects. Genome-wide DNA methylation levels of 20,687 out of 472,245 CpG sites in blood leukocytes were associated with total carotenoid concentrations. Using WGCNA, nine co-methylation modules were identified. A total of 2734 hub genes (17 unique top hub genes) were potentially related to lipid profile. This study provides evidence for the potential implications of gene co-methylation in the relationship between plasma carotenoids and lipid profile. Further studies and validation of the hub genes are needed. Full article
(This article belongs to the Special Issue Nutrition and Epigenetics)
Show Figures

Figure 1

Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Author: Paolo Garagnani
Affiliation: Department of Experimental, Diagnostic, and Specialty Medicine (DIMES), University of Bologna, Italy
Title: Epigenetic readouts of dietary interventions

Author: Mauro Provinciali
Affiliation: Italian National Research Center on Ageing (INRCA), Ancona, Italy
Title: Circulating markers of nutritional status and CpG DNA methylation in young and elderly subjects

Author: Giuseppe Passarino
Affiliation: Department of Biology, Ecology and Earth Science, University of Calabria, Rende, Italy
Title: Tissue specific epigenetic modifications of mitochondrial correlated genes in relation to aging and diet

Author: Celine Tiffon
Affiliation: French National Cancer Institute, Boulogne-Billancourt, France
Title: Nutrition-related epigenetic modifications: characterization on metabolism, aging and health status

Back to TopTop