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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 2026) | Viewed by 16539

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Dr. Lusânia Maria Greggi Antunes

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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
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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

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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 (9 papers)

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Research

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12 pages, 561 KB

Open AccessArticle

Sweet Taste Receptor Genetic Variation TAS1R2 rs35874116 Is Associated with Dietary Quality in a Korean Population

by Eunyoung Kim and Jeong-Hwa Choi

Nutrients 2026, 18(8), 1224; https://doi.org/10.3390/nu18081224 - 14 Apr 2026

Viewed by 319

Abstract

Background/Objectives: Individual differences in sweet taste sensitivity, influenced by genetic factors such as variants of the taste receptor type 1 member 2 (TAS1R2), are associated with food preferences and nutrient intake. However, the relationship between TAS1R2 polymorphisms and diet quality in Koreans remains unexplored. This study investigated the association between the TAS1R2 rs35874116 (T>C, Ile191Val) variant and diet quality, assessed using the Korean Healthy Eating Index (KHEI). Methods: Analyzing data from the Korean Genome and Epidemiology Study, we evaluated the dietary quality of 41,669 Koreans based on KHEI scores and TAS1R2 rs35874116 genotypes (TT versus CT+CC). Results: The findings indicate that genetic variation in the sweet taste receptor is linked to specific components of dietary quality. Although total KHEI scores did not differ between genotypes, TT genotype carriers had significantly higher vegetable intake scores compared to C allele carriers (3.42 ± 1.35 vs. 3.37 ± 1.36, p_adjusted = 0.002). Additionally, TT carriers exhibited higher sodium intake (6.85 ± 3.53 vs. 6.95 ± 3.51, p_adjusted = 0.002) and lower scores in the moderation domain (18.82 ± 5.15 vs. 18.98 ± 5.07, p_adjusted = 0.002). Conclusions: The TAS1R2 rs35874116 variant is associated with specific aspects of diet quality in Koreans, particularly vegetable and sodium intake. These findings suggest that genetic variations in sweet taste perception influence dietary behaviors among Koreans. Full article

(This article belongs to the Special Issue Advances in Gene–Diet Interactions and Human Health)

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20 pages, 858 KB

Open AccessArticle

Exploring the Association Between DTC Obesity-Related Gene Polymorphisms and Obesity Risk Factors in Koreans: Focus on BDNF

by Jiha Kim, Soyoun Lee and Myoungsook Lee

Nutrients 2026, 18(4), 655; https://doi.org/10.3390/nu18040655 - 16 Feb 2026

Viewed by 552

Abstract

Background/Objectives: Among more than 300 candidate genes for obesity, FTO, MC4R, and BDNF have been approved for DTC genetic testing. However, population-specific evidence supporting their relevance to obesity-related phenotypes in Koreans remains limited. Methods: A total of 231 healthy adults aged 19–64 years were recruited between March and May 2024. Anthropometric and clinical measurements, genotyping, dietary intake, and questionnaires on socioeconomic status, family history, and lifestyle behaviors were obtained. Associations between genotypes and obesity-related phenotypes were evaluated using ANOVA and ANCOVA, multivariable-adjusted models and multicollinearity analysis-based stepwise regression. Results: In Koreans, MAFs for FTO (3 SNPs), MC4R rs17782313 and BDNF rs6265 were 13–16%, 27.1% and 47.4%, respectively. OB frequency (%) differed significantly between BDNF GG and A allele carriers (p < 0.05). Compared to GG, BDNF A allele carriers showed higher WHR, ALT, HbA1c and sodium intake (p < 0.05). BDNF A allele carriers were observed to have higher drinking frequency and elevated ALT levels. Significant genotype–obesity interactions were identified for RMR/BW status, dietary fiber, Vit E, folate, P, K, cholesterol, and PUFA (p < 0.05). Among A allele carriers, OB-related indicators (BMI, RMR, WHR) were independently associated with age, sex, RMR, SBP, ALT, leptin, and dietary intakes of Vit A and sugars. Conclusions: These findings support the relevance of BDNF rs6265 in obesity phenotypes among Korean adults and provide Korean-specific evidence for genotype-based nutrition strategies. Given the cross-sectional study, the interpretation of personalized nutrition approaches for genetic risk carriers should be made with caution. Full article

(This article belongs to the Special Issue Advances in Gene–Diet Interactions and Human Health)

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15 pages, 390 KB

Open AccessArticle

Associations of FTO and CLOCK Genetic Variants with Emotional Eating and Reward-Related Appetite Regulation Among Healthy Young Adult Males: An Exploratory Secondary Analysis

by Julie E. Brown, Christopher P. Hedges, Lindsay D. Plank and Andrea J. Braakhuis

Nutrients 2026, 18(3), 400; https://doi.org/10.3390/nu18030400 - 26 Jan 2026

Viewed by 594

Abstract

Background: Patterns of dysregulated eating, including overeating, frequent snacking, and heightened food cravings, are associated with an increased risk of obesity and metabolic disease. Eating behaviors are multidimensional and can influence many factors, including social, cultural, and biological processes. Emerging evidence suggests that genetic variation may contribute to inter-individual differences in appetite regulation and reward-related eating, potentially influencing susceptibility to dysregulated eating patterns and behaviors. Objectives: This exploratory, secondary analysis investigated possible relationships between the genetic variants FTO rs9939609, CLOCK rs1801260, MC4R rs17782313, and CD36 rs1761667 and eating behavior traits and postprandial appetite regulation in healthy young males. Methods: Thirty healthy males (27.7 ± 3.6 y; BMI 24.5 ± 2.7 kg/m²) completed the Three-Factor Eating Questionnaire (TFEQ-R18) and consumed a standardized burrito-style meal, with appetite tracked over four hours using visual analogue scales (VAS). VAS data were baseline-adjusted and summarized as incremental area under the curve (AUC) to generate two derived exploratory composites of appetite suppression and cravings suppression. Genotyping was performed using iPLEX MassARRAY, and associations were tested with ANOVA and linear regression models. Results: FTO rs9939609 was significantly associated with higher emotional eating scores (β = 11.67; 95% CI 3.50, 19.83; p = 0.007, unadjusted), and this association remained significant after false discovery rate (FDR) correction. CLOCK rs1801260 showed a nominal association with reduced postprandial cravings suppression (β = −59.17; 95% CI −104.98, −13.35; p = 0.013, unadjusted). No associations were observed for MC4R or CD36. Conclusions: This exploratory analysis found a strong association between FTO rs9939609 and emotional eating, as well as a nominal relationship between CLOCK rs1801260 and craving regulation. These findings should be interpreted as hypothesis-generating and require confirmation in larger cohorts. Full article

(This article belongs to the Special Issue Advances in Gene–Diet Interactions and Human Health)

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20 pages, 2628 KB

Open AccessArticle

Impact of Mango Bagasse and Peel Confectionery Rich in Dietary Fiber on Gut Microbiota, Metabolite Profiles, and Genetic Regulation in High-Fat-Diet-Fed Wistar Rats

by Yuritzi Barbosa, Marcela Gaytán-Martínez, Rocio Alejandra Chavez-Santoscoy, Erika Magallón-Gayón, Silvia Hinojosa-Alvarez, Adriana Chico-Peralta, Marcos de Donato and Aurea K. Ramírez-Jiménez

Nutrients 2025, 17(23), 3780; https://doi.org/10.3390/nu17233780 - 2 Dec 2025

Cited by 1 | Viewed by 1060

Abstract

Background/Objectives: Insufficient dietary fiber intake contributes to gut microbiota dysbiosis, systemic inflammation, and the onset of obesity-related metabolic disorders. Agro-industrial by-products have emerged as sustainable sources to restore microbial and metabolic balance. This study aimed to evaluate the effects of a mango bagasse- and peel-based confectionery (MC) on gut microbiota composition, short-chain fatty acids (SCFAs), and hepatic gene expression in Wistar rats fed either a standard diet (STD) or a high-fat diet (HFD). Methods: Twenty-four rats were randomly assigned to four groups (STD, MC-STD, HFD, MC-HFD) and treated for 11 weeks. Eating behavior, body composition, microbiota composition, SCFAs, and hepatic transcriptomics were evaluated. Results: MC supplementation did not significantly alter weight gain or SCFA levels but shifted clustering patterns in principal component analysis, indicating a distinct dietary response. Microbiota analysis revealed a trend toward lower relative abundances of obesogenic species such as Phascolarctobacterium faecium and Ruminococcus torques, while Intestimonas butyriciproducens and Anaerostipes hadrus were modulated according to diet type. Transcriptomic profiling demonstrated consistent downregulation of lipid metabolism–related genes (Cyp4a14, Hmgcs1, Cyp51, Fads1), linked to PPAR signaling pathways. Conclusions: MC supplementation may beneficially modulate the gut–liver axis and highlights the nutritional potential of fruit by-products as functional ingredients to promote metabolic health under high-fat dietary conditions. Full article

(This article belongs to the Special Issue Advances in Gene–Diet Interactions and Human Health)

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18 pages, 3782 KB

Open AccessArticle

Toxigenomic Evaluation of Diallyl Disulfide Effects and Its Association with the Chemotherapeutic Agent 5-Fluorouracil in Colorectal Cancer Cell Lines

by Estefani Maria Treviso, Caroline Andolfato Sanchez, Cecília Cristina Souza Rocha, Alexandre Ferro Aissa and Lusânia Maria Greggi Antunes

Nutrients 2025, 17(15), 2412; https://doi.org/10.3390/nu17152412 - 24 Jul 2025

Cited by 1 | Viewed by 1303

Abstract

Background/Objectives: Colorectal cancer (CRC) is among the most prevalent malignant neoplasms globally. Chemotherapeutic treatment strategies have demonstrated minimal improvement over the past decade. Combination therapies, including those with nutraceuticals, are currently being investigated as promising alternatives to enhance therapeutic efficacy. The organosulfur garlic extract diallyl disulfide (DADS) has demonstrated anti-tumoral activity in several types of cancer. This study aimed to investigate the effects of DADS and 5-fluorouracil (5-FU), both individually and in combination, on the human CRC cell lines Caco-2 and HT-29. Methods: Caco-2, HT-29, and non-tumoral human umbilical vein endothelial cells (HUVEC) were exposed to DADS (25–600 µM) and 5-FU (5–100 µM), either individually or in simultaneous combination (DADS 100 µM + 5-FU 100 µM), for 24 h. Cytotoxicity was evaluated in all three cell lines. In addition, the effects of these treatments on oxidative stress, cell migration, genotoxicity, cell death, global DNA methylation, and gene–nutraceutical interactions were assessed in both tumor cell lines. Results: DADS demonstrated cytotoxic effects at high concentrations in Caco-2, HT-29, and HUVECs and induced DNA damage in both colorectal cancer cell lines. The combination of DADS and 5-FU significantly promoted apoptotic cell death, increased genotoxicity, elevated global DNA methylation, and inhibited cell migration, with these effects being particularly pronounced in HT-29 cells. Conclusions: We provide evidence that DADS combined with 5-FU is potentially useful in the therapy of CRC. However the combination of nutraceuticals and chemotherapy must consider the distinct molecular and phenotypic characteristics of each tumor cell line. Full article

(This article belongs to the Special Issue Advances in Gene–Diet Interactions and Human Health)

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25 pages, 4879 KB

Open AccessArticle

Combined Phytochemical Sulforaphane and Dietary Fiber Inulin Contribute to the Prevention of ER-Negative Breast Cancer via PI3K/AKT/MTOR Pathway and Modulating Gut Microbial Composition

by Huixin Wu, Brittany L. Witt, William J. van der Pol, Casey D. Morrow, Lennard W. Duck and Trygve O. Tollefsbol

Nutrients 2025, 17(12), 2023; https://doi.org/10.3390/nu17122023 - 17 Jun 2025

Cited by 9 | Viewed by 2421

Abstract

Background: Breast cancer (BC) is the second most common cancer among women in the United States. It has been estimated that one in eight women will be diagnosed with breast cancer in her lifetime. Various BC risk factors, such as age, physical inactivity, and smoking, play a substantial role in BC occurrence and development. Early life dietary intervention with plant-based bioactive compounds has been studied for its potential role in BC prevention. Sulforaphane (SFN), an isothiocyanate, is an antioxidant and anti-inflammatory agent extracted from broccoli sprouts (BSp) and other plants. Dietary supplementation of SFN suppresses tumor growth by inducing protective epigenetic changes and inhibiting cancer cell proliferation. Inulin, as a dietary fiber, has been studied for alleviating GI discomfort and weight loss by promoting the growth of beneficial bacteria in the gut. Objective: Early-life combinatorial treatment with both phytochemical SFN and potential prebiotic agent inulin at lower and safer dosages may confer more efficacious and beneficial effects in BC prevention. Methods: Transgenic mice representing estrogen receptor-negative BC were fed 26% (w/w) BSp and 2% (w/v) inulin supplemented in food and water, respectively. Results: The combinatorial treatment inhibited tumor growth, increased tumor onset latency, and synergistically reduced tumor weight. Gut microbial composition was analyzed between groups, where Ruminococcus, Muribaculaceae, and Faecalibaculum significantly increased, while Blautia, Turicibacter, and Clostridium sensu stricto 1 significantly decreased in the combinatorial group compared with the control group. Furthermore, combinatorial treatment induced a protective epigenetic effect by inhibiting histone deacetylases (HDACs) and DNA methyltransferases (DNMTs). Intermediates in the AKT/PI3K/MTOR pathway were significantly suppressed by the combinatorial treatment, including PI3K p85, p-AKT, p-PI3K p55, MTOR, and NF-κB. Cell cycle arrest and programmed cell death were induced by the combinatorial treatment via elevating the expression of cleaved-caspase 3 and 7 and inhibiting the expressions of CDK2 and CDK4, respectively. Orally administering F. rodentium attenuated tumor growth and induced apoptosis in a syngeneic triple-negative breast cancer (TNBC) mouse model. Conclusions: Overall, the findings suggest that early-life dietary combinatorial treatment contributed to BC prevention and may be a potential epigenetic therapy that serves as an adjunct to other traditional neoadjuvant therapies. Full article

(This article belongs to the Special Issue Advances in Gene–Diet Interactions and Human Health)

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17 pages, 6452 KB

Open AccessArticle

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

Cited by 6 | Viewed by 3368

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 (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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37 pages, 1234 KB

Open AccessReview

The Complex Gene–Carbohydrate Interaction in Type 2 Diabetes: Between Current Knowledge and Future Perspectives

by Francesca Gorini and Alessandro Tonacci

Nutrients 2025, 17(14), 2350; https://doi.org/10.3390/nu17142350 - 17 Jul 2025

Cited by 3 | Viewed by 3928

Abstract

Type 2 diabetes (T2D) represents a public health problem globally, with the highest prevalence reported among older adults. While an interplay of various determinants including genetic, epigenetic, environmental factors and unhealthy lifestyle, particularly diet, has been established to contribute to T2D development, emerging evidence supports the role of interactions between nutrients or dietary patterns and genes in the pathogenesis of this metabolic disorder. The amount, and especially the type of carbohydrates, in particular, have been correlated with the risk of non-communicable chronic disease and mortality. This narrative review aims to discuss the updated data on the complex and not fully elucidated relationship between carbohydrate–gene interactions and incidence of T2D, identifying the most susceptible genes able to modulate the dual association between carbohydrate intake and risk of developing T2D. The identification of genetic polymorphisms in response to this macronutrient represents a potentially powerful target to estimate individual risk and prevent the development of T2D in the context of personalized medicine. The postulation around novel foods potentially tailored to minimize the risks of developing T2D will pave the way for a new era into food research in relation to the safeguarding of well-being status in patients affected by, or at risk for, T2D. Full article

(This article belongs to the Special Issue Advances in Gene–Diet Interactions and Human Health)

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14 pages, 839 KB

Open AccessReview

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

Cited by 2 | Viewed by 1965

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 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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