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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 July 2024) | Viewed by 17812

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Prof. Dr. Marica Bakovic

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Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, ON, Canada
Interests: nutritional genomics; gene expression; cardiovascular disease and insulin resistance
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Dear Colleagues,

Over the past 15 years, the study of nutrigenomics has established the relationship between genes, nutrition, and disease. This exciting area of research demonstrates that nutrition is not just about preventing deficiencies; it is also a promising target for preventing and treating chronic illness such as diabetes, cancer, and neurodegenerative disorders. By identifying how nutrients modulate cellular signalling pathways, diet can be used as first line of defence against these chronic illnesses. It is critical to continue characterising genes and analysing their expression under different nutritional conditions. This research not only helps inform dietary recommendations at the individual level, but can also guide the development of public dietary guidelines, which could reduce the prevalence of chronic illness in our population.

For this Special Issue, we are looking to compile recent research on how nutrients impact genetic expression at any level. Methods of studying such impacts include, but are not limited to, transcriptomics, proteomics, and metabolomics.

Prof. Dr. Marica Bakovic
Guest Editor

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Keywords

nutrition
gene expression
nutrigenomics
epigenetics
chronic illness

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Published Papers (9 papers)

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Research

15 pages, 499 KiB

Open AccessCommunication

RNA-Seq Analysis of Pubertal Mammary Epithelial Cells Reveals Novel n-3 Polyunsaturated Fatty Acid Transcriptomic Changes in the fat-1 Mouse Model

by Connor D. C. Buchanan, Rahbika Ashraf, Lyn M. Hillyer, Wangshu Tu, Jing X. Kang, Sanjeena Subedi and David W. L. Ma

Nutrients 2024, 16(22), 3925; https://doi.org/10.3390/nu16223925 - 17 Nov 2024

Viewed by 478

Abstract

Background: The early exposure of nutrients during pubertal mammary gland development may reduce the risk of developing breast cancer later in life. Anticancer n-3 polyunsaturated fatty acids (n-3 PUFA) are shown to modulate pubertal mammary gland development; however, the mechanisms of action remain unclear. Prior work focused on effects at the whole tissue level, and little is known at the cellular level, such as at the level of mammary epithelial cells (MECs), which are implicated in cancer development. Methods: This pilot study examined the effects of lifelong n-3 PUFA exposure on the transcriptome by RNA-Seq in the isolated MECs of pubertal (6–8-week-old) female fat-1 transgenic mice capable of de novo n-3 PUFA synthesis. edgeR and DESeq2 were used separately for the differential expression analysis of RNA sequencing data followed by the Benjamani–Hochberg procedure for multiple testing correction. Results: Nine genes were found concordant and significantly different (p ≤ 0.05) by both the DESeq2 and edgeR methods. These genes were associated with multiple pathways, suggesting that n-3 PUFA stimulates estrogen-related signaling (Mlltl0, Galr3, and Nrip1) and a glycolytic profile (Soga1, Pdpr, and Uso1) while offering protective effects for immune and DNA damage responses (Glpd1, Garre1, and Rpa1) in MECs during puberty. Conclusions: This pilot study highlights the utility of RNA-Seq to better understanding the mechanistic effects of specific nutrients such as n-3 PUFA in a cell-specific manner. Thus, further studies are warranted to investigate the cell-specific mechanisms by which n-3 PUFA influences pubertal mammary gland development and breast cancer risk later in life. Full article

(This article belongs to the Special Issue Nutrition and Gene Interaction)

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13 pages, 587 KiB

Open AccessArticle

The Impact of Haplotypes of the FTO Gene, Lifestyle, and Dietary Patterns on BMI and Metabolic Syndrome in Polish Young Adult Men

by Sylwia Górczyńska-Kosiorz, Mateusz Lejawa, Marcin Goławski, Agnieszka Tomaszewska, Martyna Fronczek, Beata Maksym, Maciej Banach and Tadeusz Osadnik

Nutrients 2024, 16(11), 1615; https://doi.org/10.3390/nu16111615 - 25 May 2024

Cited by 1 | Viewed by 1141

Abstract

Background: Variants in fat mass and the obesity-associated protein (FTO) gene have long been recognized as the most significant genetic predictors of body fat mass and obesity. Nevertheless, despite the overall evidence, there are conflicting reports regarding the correlation between different polymorphisms of the FTO gene and body mass index (BMI). Additionally, it is unclear whether FTO influences metabolic syndrome (MetS) through mechanisms other than BMI’s impact. In this work, we aimed to analyze the impact of the following FTO polymorphisms on the BMI as well as MetS components in a population of young adult men. Methods: The patient group consisted of 279 Polish young adult men aged 28.92 (4.28) recruited for the MAGNETIC trial. The single-nucleotide polymorphisms (SNPs), located in the first intron of the FTO gene, were genotyped, and the results were used to identify “protective” and “risk” haplotypes and diplotypes based on the literature data. Laboratory, as well as anthropometric measurements regarding MetS, were performed. Measured MetS components included those used in the definition in accordance with the current guidelines. Data regarding dietary patterns were also collected, and principal components of the dietary patterns were identified. Results: No statistically significant correlations were identified between the analyzed FTO diplotypes and BMI (p = 0.53) or other MetS components (waist circumference p = 0.55; triglycerides p = 0.72; HDL cholesterol p = 0.33; blood glucose p = 0.20; systolic blood pressure p = 0.06; diastolic blood pressure p = 0.21). Stratification by the level of physical activity or adherence to the dietary patterns also did not result in any statistically significant result. Conclusions: Some studies have shown that FTO SNPs such as rs1421085, rs1121980, rs8050136, rs9939609, and rs9930506 have an impact on the BMI or other MetS components; nevertheless, this was not replicated in this study of Polish young adult males. Full article

(This article belongs to the Special Issue Nutrition and Gene Interaction)

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12 pages, 579 KiB

Open AccessArticle

Blood Phytosterol Concentration and Genetic Variant Associations in a Sample Population

by Leticia Garrido-Sanchez, Elisabet Leiva-Badosa, Josep Llop-Talaveron, Xavier Pintó-Sala, Toni Lozano-Andreu, Emili Corbella-Inglés, Pedro Alia-Ramos, Lluis Arias-Barquet, Josep Maria Ramon-Torrel and Maria B. Badía-Tahull

Nutrients 2024, 16(7), 1067; https://doi.org/10.3390/nu16071067 - 5 Apr 2024

Viewed by 1108

Abstract

The main objective of this study was to determine plasma levels of PS and to study SNVs rs41360247, rs4245791, rs4148217, and rs11887534 of ABCG8 and the r657152 SNV at the ABO blood group locus in a sample of a population treated at our hospital, and to determine whether these SNVs are related to plasma PS concentrations. The secondary objective was to establish the variables associated with plasma PS concentrations in adults. Participants completed a dietary habit questionnaire and a blood sample was collected to obtain the following variables: campesterol, sitosterol, sitostanol, lanosterol, stigmasterol, biochemical parameters, and the SNVs. In addition, biometric and demographic variables were also recorded. In the generalized linear model, cholesterol and age were positively associated with total PS levels, while BMI was negatively related. For rs4245791, homozygous T allele individuals showed a significantly lower campesterol concentration compared with C homozygotes, and the GG alleles of rs657152 had the lowest levels of campesterol compared with the other alleles of the SNV. Conclusions: The screening of certain SNVs could help prevent the increase in plasma PS and maybe PNALD in some patients. However, further studies on the determinants of plasma phytosterol concentrations are needed. Full article

(This article belongs to the Special Issue Nutrition and Gene Interaction)

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13 pages, 303 KiB

Open AccessArticle

Genetic Variants in CD36 Involved in Fat Taste Perception: Association with Anthropometric and Clinical Parameters in Overweight and Obese Subjects Affected by Type 2 Diabetes or Dysglycemia—A Pilot Study

by Marica Franzago, Paola Borrelli, Marta Di Nicola, Liborio Stuppia and Ester Vitacolonna

Nutrients 2023, 15(21), 4656; https://doi.org/10.3390/nu15214656 - 3 Nov 2023

Cited by 2 | Viewed by 1453

Abstract

Obesity and overweight represent a growing health problem worldwide. Genes regulating the intake and metabolism of different nutrients can positively or negatively influence the efficacy of nutritional interventions against obesity and its complications. The aim of this study was to assess changes in anthropometric and clinical parameters and the adherence to a Mediterranean diet (MedDiet) over time in relation to nutrigenetic variants in overweight or obese subjects affected by Type 2 Diabetes (T2D) or dysglycemia, who were included in a nutritional program. A total of 23 subjects were included in this study. Clinical parameters, physical activity levels, and the adherence to a MedDiet were evaluated at baseline, at 6 (T6), and at 12 months (T12) during and after a diet/lifestyle intervention. In a single blood sample from each subject, rs1984112 (A>G) and rs1761667 (G>A) in CD36; rs7950226 (G>A) in BMAL1; and rs1801260 (A>G), rs4864548 (A>G), and rs3736544 (G>A) in CLOCK were genotyped with Real-Time PCR. Significant associations were observed between CD36 rs1761667 and weight (p = 0.025), hip circumference (p = 0.042), triglycerides (p = 0.047), and HbA1c (p = 0.012) at baseline. Moreover, the genotype AA in CD36 rs1761667 was significantly associated with a lower BMI when compared to G carriers at baseline, at T6, and also at T12. In addition, subjects with the AA genotype at CD36 rs1984112 had significantly lower levels of HbA1c (p = 0.027) than the GG and AG genotypes at baseline. These results show that variants in CD36 can have an impact on anthropometric and clinical parameters in overweight or obese subjects affected by T2D or dysglycemia, and that it might influence the success of the diet/lifestyle intervention. Full article

(This article belongs to the Special Issue Nutrition and Gene Interaction)

17 pages, 4023 KiB

Open AccessArticle

Tributyrin Mitigates Ethanol-Induced Lysine Acetylation of Histone-H3 and p65-NFκB Downregulating CCL2 Expression and Consequent Liver Inflammation and Injury

by Smita S. Ghare, Benjamin T. Charpentier, Dushan T. Ghooray, Jingwen Zhang, Manicka V. Vadhanam, Sreelatha Reddy, Swati Joshi-Barve, Craig J. McClain and Shirish S. Barve

Nutrients 2023, 15(20), 4397; https://doi.org/10.3390/nu15204397 - 17 Oct 2023

Cited by 7 | Viewed by 1743

Abstract

Purpose: Chemokine-driven leukocyte infiltration and sustained inflammation contribute to alcohol-associated liver disease (ALD). Elevated hepatic CCL2 expression, seen in ALD, is associated with disease severity. However, mechanisms of CCL2 regulation are not completely elucidated. Post-translational modifications (PTMs) of proteins, particularly acetylation, modulate gene expression. This study examined the acetylation changes of promoter-associated histone-H3 and key transcription factor-NFκB in regulating hepatic CCL2 expression and subsequent inflammation and injury. Further, the effect of therapeutic modulation of the acetylation state by tributyrin (TB), a butyrate prodrug, was assessed. Methods: Hepatic CCL2 expression was assessed in mice fed control (PF) or an ethanol-containing Lieber–DeCarli (5% v/v, EF) diet for 7 weeks with or without oral administration of tributyrin (TB, 2 g/kg, 5 days/week). A chromatin immunoprecipitation (ChIP) assay evaluated promoter-associated modifications. Nuclear association between SIRT1, p300, and NFκB-p65 and acetylation changes of p65 were determined using immunoprecipitation and Western blot analyses. A Student’s t-test and one-way ANOVA determined the significance. Results: Ethanol significantly increased promoter-associated histone-H3-lysine-9 acetylation (H3K9Ac), reflecting a transcriptionally permissive state with a resultant increase in hepatic CCL2 mRNA and protein expression. Moreover, increased lysine-310-acetylation of nuclear RelA/p65 decreased its association with SIRT1, a class III HDAC, but concomitantly increased with p300, a histone acetyltransferase. This further led to enhanced recruitment of NF-κB/p65 and RNA polymerase-II to the CCL2 promoter. Oral TB administration prevented ethanol-associated acetylation changes, thus downregulating CCL2 expression, hepatic neutrophil infiltration, and inflammation/ injury. Conclusion: The modulation of a protein acetylation state via ethanol or TB mechanistically regulates hepatic CCL2 upregulation in ALD. Full article

(This article belongs to the Special Issue Nutrition and Gene Interaction)

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17 pages, 827 KiB

Open AccessArticle

Interactions between Polygenetic Variants and Lifestyle Factors in Hypothyroidism: A Hospital-Based Cohort Study

by Da Sol Kim and Sunmin Park

Nutrients 2023, 15(17), 3850; https://doi.org/10.3390/nu15173850 - 3 Sep 2023

Cited by 2 | Viewed by 2517

Abstract

Hypothyroidism is a prevalent endocrine disorder and is associated with a variety of metabolic disturbances. This study aimed to investigate the polygenic variants associated with hypothyroidism risk and the interaction of polygenic risk scores (PRS) with dietary patterns in influencing disease risk in 56,664 participants aged >40 in a hospital-based cohort. The participants were classified as having hypothyroidism (n = 870) diagnosed by a physician and no hypothyroidism (n = 55,794). Genetic variants associated with hypothyroidism were identified using a genome-wide association study (GWAS). Genetic variants interacting with each other were selected using a generalized multifactor dimensionality reduction analysis, and the PRS generated was evaluated for interaction with lifestyle parameters. Coffee, alcohol, meat intake, and a Korean balanced diet were inversely associated with hypothyroidism risk, as were selenium, copper, and manganese intakes. White blood cell (WBC) counts and serum alkaline phosphatase and triglyceride concentrations were positively associated with hypothyroidism risk, as were osteoporosis and thyroid cancer. The GMDR analysis generated a three-single nucleotide polymorphism (SNP) model comprising dual oxidase-1 (DUOX1)_rs1648314; thyroid-stimulating hormone receptor (TSHR)_rs75664963; and major histocompatibility complex, class-II, DQ Alpha-1 (HLA-DQA1)_rs17426593. The PRS derived from the three- and seven-SNP models were associated with a 2.11- and 2.32-fold increase in hypothyroidism risk, respectively. Furthermore, the PRS from the three-SNP model showed interactions with WBC counts, wherein the positive association with hypothyroidism risk was more pronounced in participants with low WBC counts than those with high WBC counts (≥4 × 10⁹ /L). Dietary patterns, such as the plant-based diet (PBD) and the Western-style diet (WSD), along with smoking status, exhibited interactions with the PRS, influencing hypothyroidism risk. In participants with a high PRS, those in the high-PBD, low-WSD, and smoker groups had a higher proportion of hypothyroidism than those in the low-PBD, high-WSD, and non-smoker groups. In conclusion, genetic variants related to immunity and thyroid hormone secretion were linked to hypothyroidism risk, and their PRS interacted with PBD and WSD intake and smoking status. These results contribute to a better understanding of hypothyroidism and its prevention strategies for precision medicine intervention. Full article

(This article belongs to the Special Issue Nutrition and Gene Interaction)

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15 pages, 748 KiB

Open AccessArticle

Association of the DNA Methylation of Obesity-Related Genes with the Dietary Nutrient Intake in Children

by Priyadarshni Patel, Vaithinathan Selvaraju, Jeganathan Ramesh Babu and Thangiah Geetha

Nutrients 2023, 15(13), 2840; https://doi.org/10.3390/nu15132840 - 22 Jun 2023

Cited by 7 | Viewed by 2478

Abstract

The occurrence of obesity stems from both genetic and external influences. Despite thorough research and attempts to address it through various means such as dietary changes, physical activity, education, and medications, a lasting solution to this widespread problem remains elusive. Nutrients play a crucial role in various cellular processes, including the regulation of gene expression. One of the mechanisms by which nutrients can affect gene expression is through DNA methylation. This modification can alter the accessibility of DNA to transcription factors and other regulatory proteins, thereby influencing gene expression. Nutrients such as folate and vitamin B12 are involved in the one-carbon metabolism pathway, which provides the methyl groups necessary for DNA methylation. Studies have shown that the inadequate intake of these nutrients can lead to alterations in DNA methylation patterns. For this study, we aim to understand the differences in the association of the dietary intake between normal weight and overweight/obese children and between European American and African American children with the DNA methylation of the three genes NRF1, FTO, and LEPR. The research discovered a significant association between the nutritional intake of 6–10-years-old children, particularly the methyl donors present in their diet, and the methylation of the NRF1, FTO, and LEPR genes. Additionally, the study emphasizes the significance of considering health inequalities, particularly family income and maternal education, when investigating the epigenetic impact of methyl donors in diet and gene methylation. Full article

(This article belongs to the Special Issue Nutrition and Gene Interaction)

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23 pages, 2903 KiB

Open AccessArticle

by Sunmin Park

Nutrients 2023, 15(7), 1764; https://doi.org/10.3390/nu15071764 - 4 Apr 2023

Cited by 5 | Viewed by 2782

Abstract

Adult height is inversely related to metabolic syndrome (MetS) risk, but its genetic impacts have not been revealed. The present study aimed to examine the hypothesis that adult height-related genetic variants interact with lifestyle to influence adult height and are associated with MetS risk in adults aged >40 in Korea during 2010–2014. Participants were divided into short stature (SS; control) and tall stature (TS; case) by the 85th percentile of adult height. The genetic variants linked to adult height were screened from a genome-wide association study in a city hospital-based cohort (n = 58,701) and confirmed in Ansan/Ansung plus rural cohorts (n = 13,783) among the Korean Genome and Epidemiology Study. Genetic variants that interacted with each other were identified using the generalized multifactor dimensionality reduction (GMDR) analysis. The interaction between the polygenic risk score (PRS) of the selected genetic variants and lifestyles was examined. Adult height was inversely associated with MetS, cardiovascular diseases, and liver function. The PRS, including zinc finger and BTB domain containing 38 (ZBTB38)_rs6762722, polyadenylate-binding protein-interacting protein-2B (PAIP2B)_rs13034890, carboxypeptidase Z (CPZ)_rs3756173, and latent-transforming growth factor beta-binding protein-1 (LTBP1)_rs4630744, was positively associated with height by 1.29 times and inversely with MetS by 0.894 times after adjusting for covariates. In expression quantitative trait loci, the gene expression of growth/differentiation factor-5 (GDF5)_rs224331, non-SMC condensin I complex subunit G (NCAPG)_rs2074974, ligand-dependent nuclear receptor corepressor like (LCORL)_rs7700107, and insulin-like growth factor-1 receptor (IGF1R)_rs2871865 was inversely linked to their risk allele in the tibial nerve and brain. The gene expression of PAIP2B_rs13034890 and a disintegrin and metalloproteinase with thrombospondin motifs-like-3 (ADAMTSL3)_rs13034890 was positively related to it. The PRS was inversely associated with MetS, hyperglycemia, HbA1c, and white blood cell counts. The wild type of GDF5_rs224331 (Ala276) lowered binding energy with rugosin A, D, and E (one of the hydrolyzable tannins) but not the mutated one (276Ser) in the in-silico analysis. The PRS interacted with energy intake and rice-main diet; PRS impact was higher in the high energy intake and the low rice-main diet. In conclusion, the PRS for adult height interacted with energy intake and diet patterns to modulate height and was linked to height and MetS by modulating their expression in the tibial nerve and brain. Full article

(This article belongs to the Special Issue Nutrition and Gene Interaction)

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13 pages, 816 KiB

Open AccessArticle

Interaction between the PNPLA3 Gene and Nutritional Factors on NAFLD Development: The Korean Genome and Epidemiology Study

by Sooyeon Oh, Jooho Lee, Sukyung Chun, Ja-Eun Choi, Mi Na Kim, Young Eun Chon, Yeonjung Ha, Seong-Gyu Hwang, Sang-Woon Choi and Kyung-Won Hong

Nutrients 2023, 15(1), 152; https://doi.org/10.3390/nu15010152 - 28 Dec 2022

Cited by 6 | Viewed by 2884

Abstract

Genetic and nutritional factors contribute to the development of non-alcoholic fatty liver disease (NAFLD); however, gene–diet interactions in NAFLD development are poorly understood. In this case–control study, a large dataset from the Korean Genome and Epidemiology Study cohort (n = 72,299) comprising genomic data, medical records, social history, and dietary data was used. We investigated the interactions between the PNPLA3 rs738409 genotype and nutritional factors and their possible effect on the risk of NAFLD development in 2950 patients with NAFLD and 12,907 controls. In the PNPLA3 risk allele group, high protein, fat, sodium, phosphorus, niacin, and vitamin B6 intakes were associated with a decreased risk of NAFLD. In the non-risk allele group, only high fat intake was associated with a decreased risk of NAFLD. Among these nutrients, high sodium intake had a significant protective interaction with the PNPLA3 genotype against NAFLD (p = 0.002). Among salty foods, only kimchi had a significant protective effect against the PNPLA3 genotype (p = 0.012). Thus, the PNPLA3 genotype is differentially associated with nutritional factors. In particular, it interacts with kimchi, a fermented vegetable dish. Therefore, fermented vegetables may serve as a tailored therapeutic food for people with the PNPLA3 risk allele. Full article

(This article belongs to the Special Issue Nutrition and Gene Interaction)

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