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Nutrition and Epigenetics

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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 (10 December 2019) | Viewed by 56966

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Prof. Dr. Giuseppe Passarino

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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

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Department of Biology, University of Calabria, 87036 Rende, Italy
Interests: epigenetics; aging; statistical genetics

Prof. Dr. Dina Bellizzi

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Department of Biology, Ecology and Earth Sciences, University of Calabria, 87036 Rende, Italy
Interests: microbiota; microbiome; epigenetics; epigenetic biomarkers; DNA methylation modifications; mitochondrial DNA methylation; aging; nutrition; multi-drug resistance
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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

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Keywords

Nutrition
Dietary habits
Epigenetics
Methylation

Published Papers (12 papers)

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18 pages, 2142 KiB

Open AccessArticle

DNA Methylation Changes are Associated with the Programming of White Adipose Tissue Browning Features by Resveratrol and Nicotinamide Riboside Neonatal Supplementations in Mice

by Alba Serrano, Madhu Asnani-Kishnani, Charlene Couturier, Julien Astier, Andreu Palou, Jean-François Landrier, Joan Ribot and M. Luisa Bonet

Nutrients 2020, 12(2), 461; https://0-doi-org.brum.beds.ac.uk/10.3390/nu12020461 - 12 Feb 2020

Cited by 18 | Viewed by 3542

Abstract

Neonatal supplementation with resveratrol (RSV) or nicotinamide riboside (NR) programs in male mice brown adipocyte-like features in white adipose tissue (WAT browning) together with improved metabolism in adulthood. We tested the involvement in this programming of long-term epigenetic changes in two browning-related genes that are overexpressed in WAT of supplemented mice, Slc27a1 and Prdm16. Suckling mice received orally the vehicle, RSV or NR from postnatal days 2-to-20. After weaning (d21) onto a chow diet, male mice were habituated to a normal-fat diet (NFD) starting d75, and split on d90 into continuation on the NFD or switching to a high-fat diet (HFD) until euthanization on d164. CpG methylation by bisulfite-sequencing was analyzed on inguinal WAT. Both treatments modified methylation marks in Slc27a1 and Prdm16 and the HFD-dependent dynamics of these marks in the adult WAT, with distinct and common effects. The treatments also affected gene expression of de novo DNA methylases in WAT of young animals (euthanized at d35 in independent experiments). Studies in 3T3-L1 adipocytes indicated the direct effects of RSV and NR on the DNA methylation machinery and favoring browning features. The results support epigenetic effects being involved in WAT programming by neonatal RSV or NR supplementation in male mice. Full article

(This article belongs to the Special Issue Nutrition and Epigenetics)

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13 pages, 974 KiB

Open AccessArticle

Multi-Tissue DNA Methylation Remodeling at Mitochondrial Quality Control Genes According to Diet in Rat Aging Models

by Patrizia D’Aquila, Francesco De Rango, Francesco Guarasci, Maurizio Mandalà, Andrea Corsonello, Dina Bellizzi and Giuseppe Passarino

Nutrients 2020, 12(2), 460; https://0-doi-org.brum.beds.ac.uk/10.3390/nu12020460 - 12 Feb 2020

Cited by 7 | Viewed by 2812

Abstract

An adequate mitochondrial quality control system ensures the maintenance of a healthy mitochondrial pool so as to slow down the progressive accumulation of damage affecting mitochondrial function during aging and diseases. The amount and quality of nutrients availability were demonstrated to induce a process of bioenergetics adaptation by influencing the above system via epigenetic modifications. Here, we analyzed DNA samples from differently-aged rats fed a standard or low-calorie diet to evaluate tissue-specific changes in DNA methylation of CpG sites falling within Polg, Polg2, Tfam, Fis1, and Opa1 genes. We found significant changes according to age and tissue type and the administration of the low-calorie diet is responsible for a prevalent increase in DNA methylation levels. Particularly, this increase was more appreciable when this diet was administered during adulthood and at old age. Regression analysis demonstrated that DNA methylation patterns of the analyzed genes were negatively correlated with their expression levels. Data we obtained provide the first evidence about changes in DNA methylation patterns of genes involved in the mitochondrial biogenesis in response to specific diets and demonstrated that epigenetic modifications are involved in the modulation of mitochondrial dynamics driven by age and nutrition. Full article

(This article belongs to the Special Issue Nutrition and Epigenetics)

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15 pages, 2077 KiB

Open AccessArticle

Expression Patterns of Muscle-Specific miR-133b and miR-206 Correlate with Nutritional Status and Sarcopenia

by Francesca Iannone, Alberto Montesanto, Erika Cione, Paolina Crocco, Maria Cristina Caroleo, Serena Dato, Giuseppina Rose and Giuseppe Passarino

Nutrients 2020, 12(2), 297; https://0-doi-org.brum.beds.ac.uk/10.3390/nu12020297 - 22 Jan 2020

Cited by 32 | Viewed by 3314

Abstract

Sarcopenia and malnutrition are commonly occurring conditions in the elderly that frequently coexist, leading to substantial effects on morbidity/mortality. Evidence established muscle-specific microRNAs (miRNAs) or myomiRs as essential regulators of skeletal muscle processes, from myogenesis to muscle homeostasis. This study aimed to evaluate the association between myomiRs and sarcopenia and explore the potential of nutrition in mediating this association. qPCR was employed to characterize the myomiR-1, -133a/b, -206, -208b, and -499 expression profiles of 109 non-sarcopenic and 109 sarcopenic subjects. In our sample, the proportion malnourished or at-risk subjects was higher in sarcopenia (p < 0.001). Among the detected myomiRs (miR-133a/b and miR-206), lower levels of miR-133b was significantly associated with the presence of sarcopenia (p = 0.006); however, this relationship was not independent from nutritional status in multivariate analysis, suggesting a mediating effect of nutrition on the relationship between miR-133b and sarcopenia. Correlation analyses showed that lower miR-133b levels were associated with poor nutritional status (Mini Nutritional Assessment Long Form (MNA-LF) score, p = 0.005); furthermore, correlations with albumin, ferritin, and iron were found. Similar results were obtained for miR-206. Statistically more significant correlations were observed in subjects with sarcopenia. In conclusion, our findings highlight a nutrient-miR-133b/miR-206 pathway having a potential role in the age-related muscle decline. Full article

(This article belongs to the Special Issue Nutrition and Epigenetics)

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13 pages, 2715 KiB

Open AccessArticle

Aging and Caloric Restriction Modulate the DNA Methylation Profile of the Ribosomal RNA Locus in Human and Rat Liver

by Noémie Gensous, Francesco Ravaioli, Chiara Pirazzini, Roberto Gramignoli, Ewa Ellis, Gianluca Storci, Miriam Capri, Stephen Strom, Ezio Laconi, Claudio Franceschi, Paolo Garagnani, Fabio Marongiu and Maria Giulia Bacalini

Nutrients 2020, 12(2), 277; https://0-doi-org.brum.beds.ac.uk/10.3390/nu12020277 - 21 Jan 2020

Cited by 12 | Viewed by 3533

Abstract

A growing amount of evidence suggests that the downregulation of protein synthesis is an adaptive response during physiological aging, which positively contributes to longevity and can be modulated by nutritional interventions like caloric restriction (CR). The expression of ribosomal RNA (rRNA) is one of the main determinants of translational rate, and epigenetic modifications finely contribute to its regulation. Previous reports suggest that hypermethylation of ribosomal DNA (rDNA) locus occurs with aging, although with some species- and tissue- specificity. In the present study, we experimentally measured DNA methylation of three regions (the promoter, the 5′ of the 18S and the 5′ of 28S sequences) in the rDNA locus in liver tissues from rats at two, four, 10, and 18 months. We confirm previous findings, showing age-related hypermethylation, and describe, for the first time, that this gain in methylation also occurs in human hepatocytes. Furthermore, we show that age-related hypermethylation is enhanced in livers of rat upon CR at two and 10 months, and that at two months a trend towards the reduction of rRNA expression occurs. Collectively, our results suggest that CR modulates age-related regulation of methylation at the rDNA locus, thus providing an epigenetic readout of the pro-longevity effects of CR. Full article

(This article belongs to the Special Issue Nutrition and Epigenetics)

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15 pages, 810 KiB

Open AccessArticle

Nutritional Factors Modulating Alu Methylation in an Italian Sample from The Mark-Age Study Including Offspring of Healthy Nonagenarians

by Robertina Giacconi, Marco Malavolta, Alexander Bürkle, María Moreno-Villanueva, Claudio Franceschi, Miriam Capri, P. Eline Slagboom, Eugène H. J. M. Jansen, Martijn E. T. Dollé, Tilman Grune, Daniela Weber, Antti Hervonen, Wolfgang Stuetz, Nicolle Breusing, Fabio Ciccarone, Michele Zampieri, Valentina Aversano, Paola Caiafa, Laura Formentini, Francesco Piacenza, Elisa Pierpaoli, Andrea Basso, Mauro Provinciali and Maurizio Cardelli Show full author list Hide full author list

Nutrients 2019, 11(12), 2986; https://0-doi-org.brum.beds.ac.uk/10.3390/nu11122986 - 06 Dec 2019

Cited by 4 | Viewed by 3711

Abstract

Alu hypomethylation promotes genomic instability and is associated with aging and age-related diseases. Dietary factors affect global DNA methylation, leading to changes in genomic stability and gene expression with an impact on longevity and the risk of disease. This preliminary study aims to investigate the relationship between nutritional factors, such as circulating trace elements, lipids and antioxidants, and Alu methylation in elderly subjects and offspring of healthy nonagenarians. Alu DNA methylation was analyzed in sixty RASIG (randomly recruited age-stratified individuals from the general population) and thirty-two GO (GeHA offspring) enrolled in Italy in the framework of the MARK-AGE project. Factor analysis revealed a different clustering between Alu CpG1 and the other CpG sites. RASIG over 65 years showed lower Alu CpG1 methylation than those of GO subjects in the same age class. Moreover, Alu CpG1 methylation was associated with fruit and whole-grain bread consumption, LDL2-Cholesterol and plasma copper. The preserved Alu methylation status in GO, suggests Alu epigenetic changes as a potential marker of aging. Our preliminary investigation shows that Alu methylation may be affected by food rich in fibers and antioxidants, or circulating LDL subfractions and plasma copper. Full article

(This article belongs to the Special Issue Nutrition and Epigenetics)

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19 pages, 4237 KiB

Open AccessArticle

mir-101-3p Downregulation Promotes Fibrogenesis by Facilitating Hepatic Stellate Cell Transdifferentiation During Insulin Resistance

by Marica Meroni, Miriam Longo, Veronica Erconi, Luca Valenti, Stefano Gatti, Anna Ludovica Fracanzani and Paola Dongiovanni

Nutrients 2019, 11(11), 2597; https://0-doi-org.brum.beds.ac.uk/10.3390/nu11112597 - 29 Oct 2019

Cited by 28 | Viewed by 4488

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 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)

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22 pages, 3042 KiB

Open AccessArticle

Maternal Low-Fat Diet Programs the Hepatic Epigenome despite Exposure to an Obesogenic Postnatal Diet

by Laura Moody, Justin Shao, Hong Chen and Yuan-Xiang Pan

Nutrients 2019, 11(9), 2075; https://0-doi-org.brum.beds.ac.uk/10.3390/nu11092075 - 03 Sep 2019

Cited by 7 | Viewed by 3407

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 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)

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14 pages, 2620 KiB

Open AccessArticle

Network Analysis of the Potential Role of DNA Methylation in the Relationship between Plasma Carotenoids and Lipid Profile

by Bénédicte L. Tremblay, Frédéric Guénard, Benoît Lamarche, Louis Pérusse and Marie-Claude Vohl

Nutrients 2019, 11(6), 1265; https://0-doi-org.brum.beds.ac.uk/10.3390/nu11061265 - 04 Jun 2019

Cited by 14 | Viewed by 3954

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 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)

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Review

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23 pages, 937 KiB

Open AccessReview

Science and Healthy Meals in the World: Nutritional Epigenomics and Nutrigenetics of the Mediterranean Diet

by Fabio Caradonna, Ornella Consiglio, Claudio Luparello and Carla Gentile

Nutrients 2020, 12(6), 1748; https://0-doi-org.brum.beds.ac.uk/10.3390/nu12061748 - 11 Jun 2020

Cited by 48 | Viewed by 7321

Abstract

The Mediterranean Diet (MD), UNESCO Intangible Cultural Heritage of Humanity, has become a scientific topic of high interest due to its health benefits. The aim of this review is to pick up selected studies that report nutrigenomic or nutrigenetic data and recapitulate some of the biochemical/genomic/genetic aspects involved in the positive health effects of the MD. These include (i) the antioxidative potential of its constituents with protective effects against several diseases; (ii) the epigenetic and epigenomic effects exerted by food components, such as Indacaxanthin, Sulforaphane, and 3-Hydroxytyrosol among others, and their involvement in the modulation of miRNA expression; (iii) the existence of predisposing or protective human genotypes due to allelic diversities and the impact of the MD on disease risk. A part of the review is dedicated to the nutrigenomic effects of the main cooking methods used in the MD and also to a comparative analysis of the nutrigenomic properties of the MD and other diet regimens and non-MD-related aliments. Taking all the data into account, the traditional MD emerges as a diet with a high antioxidant and nutrigenomic modulation power, which is an example of the “Environment-Livings-Environment” relationship and an excellent patchwork of interconnected biological actions working toward human health. Full article

(This article belongs to the Special Issue Nutrition and Epigenetics)

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22 pages, 1110 KiB

Open AccessReview

Gut Microbiota as Important Mediator Between Diet and DNA Methylation and Histone Modifications in the Host

by Patrizia D’Aquila, Laurie Lynn Carelli, Francesco De Rango, Giuseppe Passarino and Dina Bellizzi

Nutrients 2020, 12(3), 597; https://0-doi-org.brum.beds.ac.uk/10.3390/nu12030597 - 25 Feb 2020

Cited by 32 | Viewed by 6704

Abstract

The human gut microbiota is a complex ecosystem consisting of trillions of microorganisms that inhabit symbiotically on and in the human intestine. They carry out, through the production of a series of metabolites, many important metabolic functions that complement the activity of mammalian enzymes and play an essential role in host digestion. Interindividual variability of microbiota structure, and consequently of the expression of its genes (microbiome), was largely ascribed to the nutritional regime. Diet influences microbiota composition and function with short- and long-term effects. In spite of the vast literature, molecular mechanisms underlying these effects still remain elusive. In this review, we summarized the current evidence on the role exerted by gut microbiota and, more specifically, by its metabolites in the establishment of the host epigenome. The interest in this topic stems from the fact that, by modulating DNA methylation and histone modifications, the gut microbiota does affect the cell activities of the hosting organism. Full article

(This article belongs to the Special Issue Nutrition and Epigenetics)

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23 pages, 934 KiB

Open AccessReview

Epigenetics: Linking Early Postnatal Nutrition to Obesity Programming?

by Lucie Marousez, Jean Lesage and Delphine Eberlé

Nutrients 2019, 11(12), 2966; https://0-doi-org.brum.beds.ac.uk/10.3390/nu11122966 - 05 Dec 2019

Cited by 49 | Viewed by 6978

Abstract

Despite constant research and public policy efforts, the obesity epidemic continues to be a major public health threat, and new approaches are urgently needed. It has been shown that nutrient imbalance in early life, from conception to infancy, influences later obesity risk, suggesting that obesity could result from “developmental programming”. In this review, we evaluate the possibility that early postnatal nutrition programs obesity risk via epigenetic mechanisms, especially DNA methylation, focusing on four main topics: (1) the dynamics of epigenetic processes in key metabolic organs during the early postnatal period; (2) the epigenetic effects of alterations in early postnatal nutrition in animal models or breastfeeding in humans; (3) current limitations and remaining outstanding questions in the field of epigenetic programming; (4) candidate pathways by which early postnatal nutrition could epigenetically program adult body weight set point. A particular focus will be given to the potential roles of breast milk fatty acids, neonatal metabolic and hormonal milieu, and gut microbiota. Understanding the mechanisms by which early postnatal nutrition can promote lifelong metabolic modifications is essential to design adequate recommendations and interventions to “de-program” the obesity epidemic. Full article

(This article belongs to the Special Issue Nutrition and Epigenetics)

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20 pages, 1566 KiB

Open AccessReview

Is an “Epigenetic Diet” for Migraines Justified? The Case of Folate and DNA Methylation

by Michal Fila, Cezary Chojnacki, Jan Chojnacki and Janusz Blasiak

Nutrients 2019, 11(11), 2763; https://0-doi-org.brum.beds.ac.uk/10.3390/nu11112763 - 14 Nov 2019

Cited by 26 | Viewed by 6170

Abstract

Migraines are a common disease with limited treatment options and some dietary factors are recognized to trigger headaches. Although migraine pathogenesis is not completely known, aberrant DNA methylation has been reported to be associated with its occurrence. Folate, an essential micronutrient involved in one-carbon metabolism and DNA methylation, was shown to have beneficial effects on migraines. Moreover, the variability of the methylenetetrahydrofolate reductase gene, important in both folate metabolism and migraine pathogenesis, modulates the beneficial effects of folate for migraines. Therefore, migraine could be targeted by a folate-rich, DNA methylation-directed diet, but there are no data showing that beneficial effects of folate consumption result from its epigenetic action. Furthermore, contrary to epigenetic drugs, epigenetic diets contain many compounds, some yet unidentified, with poorly known or completely unknown potential to interfere with the epigenetic action of the main dietary components. The application of epigenetic diets for migraines and other diseases requires its personalization to the epigenetic profile of a patient, which is largely unknown. Results obtained so far do not warrant the recommendation of any epigenetic diet as effective in migraine prevention and therapy. Further studies including a folate-rich diet fortified with valproic acid, another modifier of epigenetic profile effective in migraine prophylaxis, may help to clarify this issue. Full article

(This article belongs to the Special Issue Nutrition and Epigenetics)

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