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Nutrients
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Advances in Gene–Diet Interactions and Human Health
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Advances in Gene–Diet Interactions and Human Health

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

Deadline for manuscript submissions: 15 July 2025 | Viewed by 1964

Special Issue Editor

Dr. Lusânia Maria Greggi Antunes

E-Mail Website
Guest Editor
School of Pharmaceutical Sciences of Ribeirao Preto, University of Sao Paulo, Sao Paulo 14049-900, Brazil
Interests: nutrigenomics; genetic toxicology; nutraceuticals; epigenetics; DNA methylation; DNA damage and cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Gene–diet interactions are an important area of research that investigates the effects of bioactive compounds present in foods, nutraceuticals, and dietary supplements on the mechanisms of gene expression regulation. Gene–diet interactions can be characterized by the modulation of transcriptomics, proteomics, metabolomics, and epigenetic mechanisms, such as the methylation of genes involved in cell signaling pathways and the carcinogenic process. The scientific literature also demonstrates the ability of diet and its compounds to act on miRNAs. Several clinical trials with dietary compounds have been completed or are underway with favorable outcomes for health promotion. Advances in research on gene–diet interactions may contribute to the elucidation of molecular mechanisms and new approaches for the treatment and prevention of human diseases.

This Special Issue, “Advances in Gene–Diet Interactions and Human Health”, welcomes research articles and review articles focused on diet, genetics, and their effect on disease.

Dr. Lusânia Maria Greggi Antunes
Guest Editor

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 submissions that pass pre-check are 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 semimonthly 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 2900 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

  • genetics
  • nutrition
  • complex diseases
  • public health
  • obesity
  • whole-genome
  • epidemiological studies
  • cardiovascular disease
  • cancer
  • diet
  • polymorphism
  • cell cycle
  • clinical trials

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Published Papers (2 papers)

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Research

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17 pages, 6452 KiB  
Article
The Impact of Tartrazine on DNA Methylation, Histone Deacetylation, and Genomic Stability in Human Cell Lines
by Afshin Zand, John M. Macharia, Istvan Szabó, Gellért Gerencsér, Ádám Molnár, Bence L. Raposa and Timea Varjas
Nutrients 2025, 17(5), 913; https://doi.org/10.3390/nu17050913 - 6 Mar 2025
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Abstract
Background/Objectives: Tartrazine (TRZ), a synthetic red azo dye derived from coal tar, is widely used as a food colorant in various food products, pharmaceuticals, and cosmetics. This study aims to investigate the impact of TRZ on the expression levels of DNA methyltransferases ( [...] Read more.
Background/Objectives: Tartrazine (TRZ), a synthetic red azo dye derived from coal tar, is widely used as a food colorant in various food products, pharmaceuticals, and cosmetics. This study aims to investigate the impact of TRZ on the expression levels of DNA methyltransferases (DNMT1, DNMT3a, and DNMT3b) and histone deacetylases (HDAC5 and HDAC6). Additionally, we evaluate genomic DNA stability using the alkaline comet assay in three human cell lines: immortalized human keratinocyte (HaCaT), human hepatocellular carcinoma (HepG2), and human lung adenocarcinoma (A549). The research question focuses on whether TRZ exposure alters epigenetic regulation and DNA integrity, potentially implicating its role in carcinogenesis. Methods: The selected human cell lines were exposed to different concentrations of TRZ (20 µM, 40 µM, and 80 µM), with DMBA serving as a positive control. After treatment, we quantified the expression levels of DNMT1, DNMT3a, DNMT3b, HDAC5, and HDAC6 using quantitative real-time PCR. Additionally, we assessed DNA fragmentation via the alkaline comet assay to determine the extent of DNA damage resulting from TRZ exposure. Results: Our findings indicate that TRZ significantly upregulates the expression of HDAC5, HDAC6, DNMT1, DNMT3a, and DNMT3b in comparison to the control group. Furthermore, TRZ exposure leads to a notable increase in DNA damage, as evidenced by elevated tail moments across all examined human cell lines. Conclusions: These results suggest that TRZ may play a role in carcinogenesis and epigenetic modifications. The observed upregulation of DNMTs and HDACs, coupled with increased DNA damage, highlights the potential risks associated with TRZ exposure. Further research is necessary to explore these mechanisms and assess their implications for human health. Full article
(This article belongs to the Special Issue Advances in Gene–Diet Interactions and Human Health)
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Review

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14 pages, 839 KiB  
Review
N6-Methyladenosine Modification in the Metabolic Dysfunction-Associated Steatotic Liver Disease
by Satoru Matsuda, Moeka Nakashima, Akari Fukumoto and Naoko Suga
Nutrients 2025, 17(7), 1158; https://doi.org/10.3390/nu17071158 - 27 Mar 2025
Viewed by 590
Abstract
Epigenetics of N6-methyladenine (m6A) modification may play a key role during the regulation of various diseases, including metabolic dysfunction-associated steatotic liver disease (MASLD). The m6A modification has been shown to be accomplished via the exploitation of several players such as methyltransferases, demethylases, and/or [...] Read more.
Epigenetics of N6-methyladenine (m6A) modification may play a key role during the regulation of various diseases, including metabolic dysfunction-associated steatotic liver disease (MASLD). The m6A modification has been shown to be accomplished via the exploitation of several players such as methyltransferases, demethylases, and/or methylation-binding molecules. Significantly, the m6A methylation can regulate the key eukaryotic transcriptome by affecting the subcellular localization, splicing, export, stability, translation, and decay of those RNAs. An increasing amount of data has designated that the m6A modification of RNAs can also modulate the expression of autophagy-related genes, which could also control the autophagy in hepatocytes. Oxidative stress with reactive oxygen species (ROS) can induce m6A RNA methylation, which might be associated with the regulation of mitochondrial autophagy (mitophagy) and/or the development of MASLD. Therefore, both autophagy and the m6A modification could play important roles in regulating the pathogenesis of MASLD. Comprehending the relationship between m6A and mitophagy may be helpful for the development of future therapeutic strategies against MASLD. This review would advance the understanding of the regulatory mechanisms of m6A RNA modification, focusing on the impact of mitochondrial dysregulation and mitophagy in the liver with MASLD. Full article
(This article belongs to the Special Issue Advances in Gene–Diet Interactions and Human Health)
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