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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 (30 June 2020) | Viewed by 38855

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Special Issue Editor

Prof. Dr. Karani S. Vimaleswaran

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Guest Editor

Hugh Sinclair Unit of Human Nutrition, Department of Food and Nutritional Sciences, University of Reading, Reading RG6 6DZ, UK
Interests: lifestyle–gene interactions; diet–gene interactions; physical activity–gene interactions; nutrigenetics; nutrigenomics; obesity; diabetes; cardiovascular disease; gut microbiome; precision nutrition; personalised nutrition
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Special Issue Information

Dear Colleagues,

The completion of human genome sequencing and the introduction of high-throughout ‘omic’ technologies have allowed a better understanding of nutrient–gene interactions that vary between genotypes with the ultimate goal of developing personalised nutrition strategies for optimal health and disease prevention.

Humans are affected by both environmental and genetic factors; both factors must be considered equally to maintain normal health condition of an individual. Previous studies were mostly directed at either the effects of environmental factors alone or at genes only but not both together. Recently, gene–nutrition interactions have been investigated. Nutrition may impact health outcomes by directly affecting the expression of genes in critical metabolic pathways. Better health outcomes can be achieved if nutritional requirements are individually tailored taking into consideration the genetic make-up, life stage, dietary preferences, and health status of a person. This area of scientific research necessitates better understanding of the mechanisms of nutrient-dependent interactions at the genetic, molecular, protein, and metabolic profile levels.

This Special Issue, “Nutrient–Gene Interactions”, welcomes manuscripts detailing human and animal studies focused on the roles of dietary and genetic factors in complex diseases such as cardiovascular disease, diabetes, cancer, inflammatory bowel disease, Alzheimer’s disease, asthma, and rheumatoid arthritis, as well as in vitro studies aimed at elucidating the potential molecular mechanisms of diet–gene interactions. Experimental papers, up-to-date review articles, and commentaries are all welcome.

Prof. Dr. Karani S. Vimaleswaran
Guest Editor

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Keywords

nutrient–gene interactions
nutrigenetics
obesity
diabetes
cardiovascular disease
cancer
omics

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Published Papers (7 papers)

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Research

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18 pages, 651 KiB

Open AccessArticle

Interaction between Metabolic Genetic Risk Score and Dietary Fatty Acid Intake on Central Obesity in a Ghanaian Population

by Sooad Alsulami, David A. Nyakotey, Kamila Dudek, Abdul-Malik Bawah, Julie A. Lovegrove, Reginald A. Annan, Basma Ellahi and Karani Santhanakrishnan Vimaleswaran

Nutrients 2020, 12(7), 1906; https://doi.org/10.3390/nu12071906 - 27 Jun 2020

Cited by 12 | Viewed by 4451

Abstract

Obesity is a multifactorial condition arising from the interaction between genetic and lifestyle factors. We aimed to assess the impact of lifestyle and genetic factors on obesity-related traits in 302 healthy Ghanaian adults. Dietary intake and physical activity were assessed using a 3 day repeated 24 h dietary recall and global physical activity questionnaire, respectively. Twelve single nucleotide polymorphisms (SNPs) were used to construct 4-SNP, 8-SNP and 12-SNP genetic risk scores (GRSs). The 4-SNP GRS showed significant interactions with dietary fat intakes on waist circumference (WC) (Total fat, P_interaction = 0.01; saturated fatty acids (SFA), P_interaction = 0.02; polyunsaturated fatty acids (PUFA), P_interaction = 0.01 and monounsaturated fatty acids (MUFA), P_interaction = 0.01). Among individuals with higher intakes of total fat (>47 g/d), SFA (>14 g/d), PUFA (>16 g/d) and MUFA (>16 g/d), individuals with ≥3 risk alleles had a significantly higher WC compared to those with <3 risk alleles. This is the first study of its kind in this population, suggesting that a higher consumption of dietary fatty acid may have the potential to increase the genetic susceptibility of becoming centrally obese. These results support the general dietary recommendations to decrease the intakes of total fat and SFA, to reduce the risk of obesity, particularly in individuals with a higher genetic predisposition to central obesity. Full article

(This article belongs to the Special Issue Nutrient Gene Interactions)

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16 pages, 500 KiB

Open AccessArticle

Independent and Interactive Influences of Environmental UVR, Vitamin D Levels, and Folate Variant MTHFD1-rs2236225 on Homocysteine Levels

by Patrice Jones, Mark Lucock, Charlotte Martin, Rohith Thota, Manohar Garg, Zoe Yates, Christopher J. Scarlett, Martin Veysey and Emma Beckett

Nutrients 2020, 12(5), 1455; https://doi.org/10.3390/nu12051455 - 18 May 2020

Cited by 8 | Viewed by 5004

Abstract

Elevated homocysteine (Hcy) levels are a risk factor for vascular diseases. Recently, increases in ultraviolet radiation (UVR) have been linked to decreased Hcy levels. This relationship may be mediated by the status of UVR-responsive vitamins, vitamin D and folate, and/or genetic variants influencing their levels; however, this has yet to be examined. Therefore, the independent and interactive influences of environmental UVR, vitamin D and folate levels and related genetic variants on Hcy levels were examined in an elderly Australian cohort (n = 619). Red blood cell folate, 25-hydroxyvitamin D (25(OH)D), and plasma Hcy levels were determined, and genotyping for 21 folate and vitamin D-related variants was performed. Erythemal dose rate accumulated over six-weeks (6W-EDR) and four-months (4M-EDR) prior to clinics were calculated as a measure of environmental UVR. Multivariate analyses found interactions between 6W-EDR and 25(OH)D levels (p_interaction = 0.002), and 4M-EDR and MTHFD1-rs2236225 (p_interaction = 0.006) in predicting Hcy levels. The association between 6W-EDR and Hcy levels was found only in subjects within lower 25(OH)D quartiles (<33.26 ng/mL), with the association between 4M-EDR and Hcy occurring only in subjects carrying the MTHFD1-rs2236225 variant. 4M-EDR, 6W-EDR, and MTHFD1-rs2236225 were also independent predictors of Hcy. Findings highlight nutrient–environment and gene–environment interactions that could influence the risk of Hcy-related outcomes. Full article

(This article belongs to the Special Issue Nutrient Gene Interactions)

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16 pages, 1406 KiB

Open AccessArticle

A Nutrigenetic Approach to Investigate the Relationship between Metabolic Traits and Vitamin D Status in an Asian Indian Population

by Buthaina E. Alathari, Dhanasekaran Bodhini, Ramamoorthy Jayashri, Nagarajan Lakshmipriya, Coimbatore Subramanian Shanthi Rani, Vasudevan Sudha, Julie A. Lovegrove, Ranjit Mohan Anjana, Viswanathan Mohan, Venkatesan Radha, Rajendra Pradeepa and Karani S. Vimaleswaran

Nutrients 2020, 12(5), 1357; https://doi.org/10.3390/nu12051357 - 9 May 2020

Cited by 17 | Viewed by 4431

Abstract

Studies in Asian Indians have examined the association of metabolic traits with vitamin D status. However, findings have been quite inconsistent. Hence, we aimed to explore the relationship between metabolic traits and 25-hydroxyvitamin D [25(OH)D] concentrations. We investigate whether this relationship was modified by lifestyle factors using a nutrigenetic approach in 545 Asian Indians randomly selected from the Chennai Urban Rural Epidemiology Study (219 normal glucose tolerant individuals, 151 with pre-diabetes and 175 individuals with type 2 diabetes). A metabolic genetic risk score (GRS) was developed using five common metabolic disease-related genetic variants. There was a significant interaction between metabolic GRS and carbohydrate intake (energy%) on 25(OH)D (P_interaction = 0.047). Individuals consuming a low carbohydrate diet (≤62%) and those having lesser number of metabolic risk alleles (GRS ≤ 1) had significantly higher levels of 25(OH)D (p = 0.033). Conversely, individuals consuming a high carbohydrate diet despite having lesser number of risk alleles did not show a significant increase in 25(OH)D (p = 0.662). In summary, our findings show that individuals carrying a smaller number of metabolic risk alleles are likely to have higher 25(OH)D levels if they consume a low carbohydrate diet. These data support the current dietary carbohydrate recommendations of 50%–60% energy suggesting that reduced metabolic genetic risk increases 25(OH)D. Full article

(This article belongs to the Special Issue Nutrient Gene Interactions)

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18 pages, 523 KiB

Open AccessArticle

Food Intervention with Folate Reduces TNF-α and Interleukin Levels in Overweight and Obese Women with the MTHFR C677T Polymorphism: A Randomized Trial

by Jéssica Vanessa de Carvalho Lisboa, Marina Ramalho Ribeiro, Rafaella Cristhine Pordeus Luna, Raquel Patrícia Ataíde Lima, Rayner Anderson Ferreira do Nascimento, Mussara Gomes Cavalcante Alves Monteiro, Keylha Querino de Farias Lima, Carla Patrícia Novaes dos Santos Fechine, Naila Francis Paulo de Oliveira, Darlene Camati Persuhn, Robson Cavalcante Veras, Maria da Conceição Rodrigues Gonçalves, Flávia Emília Leite de Lima Ferreira, Roberto Teixeira Lima, Alexandre Sérgio da Silva, Alcides da Silva Diniz, Aléssio Tony Cavalcanti de Almeida, Ronei Marcos de Moraes, Eliseu Verly Junior and Maria José de Carvalho Costa

Nutrients 2020, 12(2), 361; https://doi.org/10.3390/nu12020361 - 30 Jan 2020

Cited by 21 | Viewed by 6103

Abstract

Methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism associated with body fat accumulation could possibly trigger an inflammatory process by elevating homocysteine levels and increasing cytokine production, causing several diseases. This study aimed to evaluate the effects of food intervention, and not folate supplements, on the levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) in overweight and obese women with the MTHFR C677T polymorphism. A randomized, double-blind eight-week clinical trial of 48 overweight and obese women was conducted. Participants were randomly assigned into two groups. They received 300 g of vegetables daily for eight weeks containing different doses of folate: 95 µg/day for Group 1 and 191 µg/day for Group 2. MTHFR C677T polymorphism genotyping was assessed by digestion with HinfI enzyme and on 12% polyacrylamide gels. Anthropometric measurements, 24-h dietary recall, and biochemical analysis (blood folic acid, vitamin B12, homocysteine (Hcy), TNF-α, IL-1β, and IL-6) were determined at the beginning and end of the study. Group 2 had a significant increase in folate intake (p < 0.001) and plasma folic acid (p < 0.05) for individuals with the cytosine–cytosine (CC), cytosine–thymine (CT), and thymine–thymine (TT) genotypes. However, only individuals with the TT genotype presented reduced levels of Hcy, TNF-α, IL-6, and IL-1β (p < 0.001). Group 1 showed significant differences in folate consumption (p < 0.001) and folic acid levels (p < 0.05) for individuals with the CT and TT genotypes. Food intervention with folate from vegetables increased folic acid levels and reduced interleukins, TNF-α, and Hcy levels, mainly for individuals with the TT genotype. Full article

(This article belongs to the Special Issue Nutrient Gene Interactions)

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20 pages, 678 KiB

Open AccessArticle

Impact of the Apolipoprotein E (epsilon) Genotype on Cardiometabolic Risk Markers and Responsiveness to Acute and Chronic Dietary Fat Manipulation

by Kumari M. Rathnayake, Michelle Weech, Kim G. Jackson and Julie A. Lovegrove

Nutrients 2019, 11(9), 2044; https://doi.org/10.3390/nu11092044 - 1 Sep 2019

Cited by 10 | Viewed by 4716

Abstract

Apolipoprotein (APO) E (ε) genotype is considered to play an important role in lipid responses to dietary fat manipulation but the impact on novel cardiometabolic risk markers is unclear. To address this knowledge gap, we investigated the relationship between the APOE genotype and cardiometabolic risk markers in response to acute and chronic dietary fat intakes. Associations with fasting (baseline) outcome measures (n = 218) were determined using data from the chronic DIVAS (n = 191/195 adults at moderate cardiovascular disease risk) and acute DIVAS-2 (n = 27/32 postmenopausal women) studies examining the effects of diets/meals varying in saturated, polyunsaturated and monounsaturated (MUFA) fatty acid composition. Participants were retrospectively genotyped for APOE (rs429358, rs7412). For baseline cardiometabolic outcomes, E4 carriers had higher fasting total and low-density lipoprotein-cholesterol (LDL-C), total cholesterol: high-density lipoprotein-cholesterol (HDL-C) and LDL-C: HDL-C ratios, but lower C-reactive protein (CRP) than E3/E3 and E2 carriers (p ≤ 0.003). Digital volume pulse stiffness index was higher in E2 carriers than the E3/E3 group (p = 0.011). Following chronic dietary fat intake, the significant diet × genotype interaction was found for fasting triacylglycerol (p = 0.010), with indication of a differential responsiveness to MUFA intake between the E3/E3 and E4 carriers (p = 0.006). Test fat × genotype interactions were observed for the incremental area under the curve for the postprandial apolipoprotein B (apoB; p = 0.022) and digital volume pulse reflection index (DVP-RI; p = 0.030) responses after the MUFA-rich meals, with a reduction in E4 carriers and increase in the E3/E3 group for the apoB response, but an increase in E4 carriers and decrease in the E3/E3 group for the DVP-RI response. In conclusion, baseline associations between the APOE genotype and fasting lipids and CRP confirm previous findings, although a novel interaction with digital volume pulse arterial stiffness was observed in the fasted state and differential postprandial apoB and DVP-RI responses after the MUFA-rich meals. The reported differential impact of the APOE genotype on cardiometabolic markers in the acute and chronic state requires confirmation. Full article

(This article belongs to the Special Issue Nutrient Gene Interactions)

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16 pages, 590 KiB

Open AccessReview

Intramuscular Mechanisms Mediating Adaptation to Low-Carbohydrate, High-Fat Diets during Exercise Training

by Emily E. Howard and Lee M. Margolis

Nutrients 2020, 12(9), 2496; https://doi.org/10.3390/nu12092496 - 19 Aug 2020

Cited by 15 | Viewed by 8782

Abstract

Interest in low-carbohydrate, high-fat (LCHF) diets has increased over recent decades given the theorized benefit of associated intramuscular adaptations and shifts in fuel utilization on endurance exercise performance. Consuming a LCHF diet during exercise training increases the availability of fat (i.e., intramuscular triglyceride stores; plasma free fatty acids) and decreases muscle glycogen stores. These changes in substrate availability increase reliance on fat oxidation for energy production while simultaneously decreasing reliance on carbohydrate oxidation for fuel during submaximal exercise. LCHF diet-mediated changes in substrate oxidation remain even after endogenous or exogenous carbohydrate availability is increased, suggesting that the adaptive response driving changes in fat and carbohydrate oxidation lies within the muscle and persists even when the macronutrient content of the diet is altered. This narrative review explores the intramuscular adaptations underlying increases in fat oxidation and decreases in carbohydrate oxidation with LCHF feeding. The possible effects of LCHF diets on protein metabolism and post-exercise muscle remodeling are also considered. Full article

(This article belongs to the Special Issue Nutrient Gene Interactions)

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13 pages, 573 KiB

Open AccessReview

The Interaction between Dietary Selenium Intake and Genetics in Determining Cancer Risk and Outcome

by Shrinidhi Kadkol and Alan M. Diamond

Nutrients 2020, 12(8), 2424; https://doi.org/10.3390/nu12082424 - 12 Aug 2020

Cited by 18 | Viewed by 3682

Abstract

There is considerable interest in the trace element selenium as a possible cancer chemopreventive dietary component, but supplementation trials have not indicated a clear benefit. Selenium is a critical component of selenium-containing proteins, or selenoproteins. Members of this protein family contain selenium in the form of selenocysteine. Selenocysteine is encoded by an in-frame UGA codon recognized as a selenocysteine codon by a regulatory element, the selenocysteine insertion sequence (SECIS), in the 3′-untranslated region of selenoprotein mRNAs. Epidemiological studies have implicated several selenoprotein genes in cancer risk or outcome based on associations between allelic variations and disease risk or mortality. These polymorphisms can be found in or near the SECIS or in the selenoprotein coding sequence. These variations both function to control protein synthesis and impact the efficiency of protein synthesis in response to the levels of available selenium. Thus, an individual’s genetic makeup and nutritional intake of selenium may interact to predispose them to acquiring cancer or affect cancer progression to lethality. Full article

(This article belongs to the Special Issue Nutrient Gene Interactions)

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