Special Issue "Gene Polymorphism and Nutrition: Relationships with Chronic Disease"

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

Deadline for manuscript submissions: 31 December 2021.

Special Issue Editors

Dr. Daniel-Antonio de Luis Roman
E-Mail Website
Guest Editor
1. Servicio de Endocrinología y Nutrición, Hospital Clínico Universitario de Valladolid, Av. Ramón y Cajal, 3, 47003 Valladolid, Spain
2. Instituto de Endocrinología y Nutrición (IENVA), Universidad de Valladolid, Av. Ramón y Cajal, 3, 47003 Valladolid, Spain
Interests: obesity; nutrigenetics; enteral nutrition; malnutrition related to the disease
Dr. Ana B. Crujeiras
E-Mail Website
Guest Editor
Epigenomics in Endocrinology and Nutrition Group, Instituto de Investigacion Sanitaria (IDIS), Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS), CIBER Fisiopatologia de la Obesidad y Nutricion (CIBEROBN). Rúa da Choupana, s/n, 15706 Santiago de Compostela, A Coruña, Spain
Interests: adipose tissue; nutrition; obesity; cancer; genetics; weight loss; weight regain

Special Issue Information

Dear Colleagues,

Studies of global human genomic variation have shown important population-based differences in allele frequencies of common single nucleotide polymorphisms (SNPs) that influence the expression of genes related with nutrition and, secondarily, with chronic disease. Some SNP sites have known functions or associations with diseases or other phenotype characteristics, including nutritional deficiencies and metabolism dietary components. There are many components of human diets that, when combined with the impact of diverse genetics on the metabolism of certain nutrients, have the capacity to give rise to harmful diet–gene interactions. This situation has the potential capacity to modify molecular phenotypes and clinical phenotypes, including human disease. Obesity, diabetes mellitus, chronobiology, osteoporosis, cancer, and many diseases are a field of potential investigation in this topic area. This Special Issue will include manuscripts that focus on the complex relationship between gene polymorphism and nutrition across all physiological and chronic diseases.

Dr. Daniel-Antonio de Luis Roman
Dr. Ana B. Crujeiras
Guest Editors

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 papers will be 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 monthly 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 2400 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

  • chronic disease
  • personalized nutrition
  • single nucleotide polymorphism

Published Papers (3 papers)

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Research

Article
Vitamin D and the Risks of Depression and Anxiety: An Observational Analysis and Genome-Wide Environment Interaction Study
Nutrients 2021, 13(10), 3343; https://doi.org/10.3390/nu13103343 - 24 Sep 2021
Viewed by 1419
Abstract
Previous studies have suggested that vitamin D (VD) was associated with psychiatric diseases, but efforts to elucidate the functional relevance of VD with depression and anxiety from genetic perspective have been limited. Based on the UK Biobank cohort, we first calculated polygenic risk [...] Read more.
Previous studies have suggested that vitamin D (VD) was associated with psychiatric diseases, but efforts to elucidate the functional relevance of VD with depression and anxiety from genetic perspective have been limited. Based on the UK Biobank cohort, we first calculated polygenic risk score (PRS) for VD from genome-wide association study (GWAS) data of VD. Linear and logistic regression analysis were conducted to evaluate the associations of VD traits with depression and anxiety traits, respectively. Then, using individual genotype and phenotype data from the UK Biobank, genome-wide environment interaction studies (GWEIS) were performed to identify the potential effects of gene × VD interactions on the risks of depression and anxiety traits. In the UK Biobank cohort, we observed significant associations of blood VD level with depression and anxiety traits, as well as significant associations of VD PRS and depression and anxiety traits. GWEIS identified multiple candidate loci, such as rs114086183 (p = 4.11 × 10−8, LRRTM4) for self-reported depression status and rs149760119 (p = 3.88 × 10−8, GNB5) for self-reported anxiety status. Our study results suggested that VD was negatively associated with depression and anxiety. GWEIS identified multiple candidate genes interacting with VD, providing novel clues for understanding the biological mechanism potential associations between VD and psychiatric disorders. Full article
(This article belongs to the Special Issue Gene Polymorphism and Nutrition: Relationships with Chronic Disease)
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Article
Association Study among Comethylation Modules, Genetic Polymorphisms and Clinical Features in Mexican Teenagers with Eating Disorders: Preliminary Results
Nutrients 2021, 13(9), 3210; https://doi.org/10.3390/nu13093210 - 15 Sep 2021
Viewed by 497
Abstract
Eating disorders are psychiatric disorders characterized by disturbed eating behaviors. They have a complex etiology in which genetic and environmental factors interact. Analyzing gene-environment interactions could help us to identify the mechanisms involved in the etiology of such conditions. For example, comethylation module [...] Read more.
Eating disorders are psychiatric disorders characterized by disturbed eating behaviors. They have a complex etiology in which genetic and environmental factors interact. Analyzing gene-environment interactions could help us to identify the mechanisms involved in the etiology of such conditions. For example, comethylation module analysis could detect the small effects of epigenetic interactions, reflecting the influence of environmental factors. We used MethylationEPIC and Psycharray microarrays to determine DNA methylation levels and genotype from 63 teenagers with eating disorders. We identified 11 comethylation modules in WGCNA (Weighted Gene Correlation Network Analysis) and correlated them with single nucleotide polymorphisms (SNP) and clinical features in our subjects. Two comethylation modules correlated with clinical features (BMI and height) in our sample and with SNPs associated with these phenotypes. One of these comethylation modules (yellow) correlated with BMI and rs10494217 polymorphism (associated with waist-hip ratio). Another module (black) was correlated with height, rs9349206, rs11761528, and rs17726787 SNPs; these polymorphisms were associated with height in previous GWAS. Our data suggest that genetic variations could alter epigenetics, and that these perturbations could be reflected as variations in clinical features. Full article
(This article belongs to the Special Issue Gene Polymorphism and Nutrition: Relationships with Chronic Disease)
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Article
Adiponectin Gene Variant rs3774261, Effects on Lipid Profile and Adiponectin Levels after a High Polyunsaturated Fat Hypocaloric Diet with Mediterranean Pattern
Nutrients 2021, 13(6), 1811; https://doi.org/10.3390/nu13061811 - 26 May 2021
Viewed by 636
Abstract
The role of ADIPOQ gene variants on metabolic improvements after weight change secondary to different hypocaloric diets remained unclear. We evaluate the effect of rs3774261 of ADIPOQ gene polymorphism on biochemical improvements and weight change after high polyunsaturated fat hypocaloric diet with a [...] Read more.
The role of ADIPOQ gene variants on metabolic improvements after weight change secondary to different hypocaloric diets remained unclear. We evaluate the effect of rs3774261 of ADIPOQ gene polymorphism on biochemical improvements and weight change after high polyunsaturated fat hypocaloric diet with a Mediterranean dietary pattern for 12 weeks. A population of 361 obese subjects was enrolled in an intervention trial with a calorie restriction of 500 calories over the usual intake and 45.7% of carbohydrates, 34.4% of fats, and 19.9% of proteins. The percentages of different fats was; 21.8% of monounsaturated fats, 55.5% of saturated fats, and 22.7% of polyunsaturated fats. Before and after intervention, an anthropometric study, an evaluation of nutritional intake and a biochemical evaluation were realized. All patients lost weight regardless of genotype and diet used. After 12 weeks with a similar improvement in weight loss (AA vs. AG vs. GG); total cholesterol (delta: −28.1 ± 2.1 mg/dL vs. −14.2 ± 4.1 mg/dL vs. −11.0 ± 3.9 mg/dL; p = 0.02), LDL cholesterol (delta: −17.1 ± 2.1 mg/dL vs. −6.1 ± 1.9 mg/dL vs. −6.0 ± 2.3 mg/dL; p = 0.01), triglyceride levels (delta: −35.0 ± 3.6 mg/dL vs. 10.1 ± 3.2 mg/dL vs. −9.7 ± 3.1 mg/dL; p = 0.02), C reactive protein (CRP) (delta: −2.3 ± 0.1 mg/dL vs. −0.2 ± 0.1 mg/dL vs. −0.2 ± 0.1 mg/dL; p = 0.02), serum adiponectin (delta: 11.6 ± 2.9 ng/dL vs. 2.1 ± 1.3 ng/dL vs. 3.3 ± 1.1 ng/dL; p = 0.02) and adiponectin/leptin ratio (delta: 1.5 ± 0.1 ng/dL vs. 0.3 ± 0.2 ng/dL vs. 0.4 ± 0.3 ng/dL; p = 0.03), improved only in AA group. AA genotype of ADIPOQ variant (rs3774261) is related with a significant increase in serum levels of adiponectin and ratio adiponectin/leptin and decrease on lipid profile and C-reactive protein (CRP). Full article
(This article belongs to the Special Issue Gene Polymorphism and Nutrition: Relationships with Chronic Disease)
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