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Nutritional Genomics—Fundamental and Clinical Aspects

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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 (19 November 2021) | Viewed by 8367

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Prof. Dr. Ondřej Šeda

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Institute of Biology and Medical Genetics, First Faculty of Medicine, Charles University, and the General University Hospital Albertov 4, 12800 Prague 2, Czech Republic
Interests: nutrigenetics, nutrigenomics, metabolic syndrome, animal models, systems biology

Special Issue Information

Dear Colleagues,

The effects of specific nutrients and dietary regimens depend, among other factors, on the genetic composition of the individual. The goal of this Special Issue, “Nutritional Genomics—Fundamental and Clinical Aspects”, is to bring the nutrigenetic interactions and biologically and clinically relevant nutrigenomic profiles into the center of attention.

More specifically, the aim is to present the effects of interactions between gene variants and specific nutrients or diet compositions, both on the level of fundamental biological processes and the risk or clinical presentation of many conditions.

The Special Issue will thus increase our understanding of systemic consequences of specific nutrition/genome combinations and provide new evidence within a framework of personalized nutrition.

Prof. Dr. Ondřej Šeda
Guest Editor

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Keywords

Gene-diet interaction
Nutrigenomics
Association study
Personalized nutrition
Animal models
Polygenic risk scores and nutrition

Published Papers (3 papers)

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Research

11 pages, 1405 KiB

Open AccessFeature PaperArticle

Nutrigenetic Interaction of Spontaneously Hypertensive Rat Chromosome 20 Segment and High-Sucrose Diet Sensitizes to Metabolic Syndrome

by Ondřej Šeda, Kristýna Junková, Hana Malinska, Adéla Kábelová, Martina Hüttl, Michaela Krupková, Irena Markova, František Liška and Lucie Šedová

Nutrients 2022, 14(16), 3428; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14163428 - 20 Aug 2022

Viewed by 1747

Abstract

Several corresponding regions of human and mammalian genomes have been shown to affect sensitivity to the manifestation of metabolic syndrome via nutrigenetic interactions. In this study, we assessed the effect of sucrose administration in a newly established congenic strain BN.SHR20, in which a limited segment of rat chromosome 20 from a metabolic syndrome model, spontaneously hypertensive rat (SHR), was introgressed into Brown Norway (BN) genomic background. We mapped the extent of the differential segment and compared the genomic sequences of BN vs. SHR within the segment in silico. The differential segment of SHR origin in BN.SHR20 spans about 9 Mb of the telomeric portion of the short arm of chromosome 20. We identified non-synonymous mutations e.g., in ApoM, Notch4, Slc39a7, Smim29 genes and other variations in or near genes associated with metabolic syndrome in human genome-wide association studies. Male rats of BN and BN.SHR20 strains were fed a standard diet for 18 weeks (control groups) or 16 weeks of standard diet followed by 14 days of high-sucrose diet (HSD). We assessed the morphometric and metabolic profiles of all groups. Adiposity significantly increased only in BN.SHR20 after HSD. Fasting glycemia and the glucose levels during the oral glucose tolerance test were higher in BN.SHR20 than in BN groups, while insulin levels were comparable. The fasting levels of triacylglycerols were the highest in sucrose-fed BN.SHR20, both compared to the sucrose-fed BN and the control BN.SHR20. The non-esterified fatty acids and total cholesterol concentrations were higher in BN.SHR20 compared to their respective BN groups, and the HSD elicited an increase in non-esterified fatty acids only in BN.SHR20. In a new genetically defined model, we have isolated a limited genomic region involved in nutrigenetic sensitization to sucrose-induced metabolic disturbances. Full article

(This article belongs to the Special Issue Nutritional Genomics—Fundamental and Clinical Aspects)

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20 pages, 1287 KiB

Open AccessArticle

Interactions between Polygenic Risk Scores, Dietary Pattern, and Menarche Age with the Obesity Risk in a Large Hospital-Based Cohort

by Sunmin Park, Hye Jeong Yang, Min Jung Kim, Haeng Jeon Hur, Soon-Hee Kim and Myung-Sunny Kim

Nutrients 2021, 13(11), 3772; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13113772 - 25 Oct 2021

Cited by 14 | Viewed by 2954

Abstract

Obese Asians are more susceptible to metabolic diseases than obese Caucasians of the same body mass index (BMI). We hypothesized that the genetic variants associated with obesity risk interact with the lifestyles of middle-aged and elderly adults, possibly allowing the development of personalized interventions based on genotype. We aimed to examine this hypothesis in a large city hospital-based cohort in Korea. The participants with cancers, thyroid diseases, chronic kidney disease, or brain-related diseases were excluded. The participants were divided into case and control according to their BMI: ≥25 kg/m² (case; n = 17,545) and <25 kg/m² (control; n = 36,283). The genetic variants that affected obesity risk were selected using a genome-wide association study, and the genetic variants that interacted with each other were identified by generalized multifactor dimensionality reduction analysis. The selected genetic variants were confirmed in the Ansan/Ansung cohort, and polygenetic risk scores (PRS)−nutrient interactions for obesity risk were determined. A high BMI was associated with a high-fat mass (odds ratio (OR) = 20.71) and a high skeletal muscle-mass index (OR = 3.38). A high BMI was positively related to metabolic syndrome and its components, including lipid profiles, whereas the initial menstruation age was inversely associated with a high BMI (OR = 0.78). The best model with 5-SNPs included SEC16B_rs543874, DNAJC27_rs713586, BDNF_rs6265, MC4R_rs6567160, and GIPR_rs1444988703. The high PRS with the 5-SNP model was positively associated with an obesity risk of 1.629 (1.475–1.798) after adjusting for the covariates. The 5-SNP model interacted with the initial menstruation age, fried foods, and plant-based diet for BMI risk. The participants with a high PRS also had a higher obesity risk when combined with early menarche, low plant-based diet, and a high fried-food intake than in participants with late menarche, high plant-based diet, and low fried-food intake. In conclusion, people with a high PRS and earlier menarche age are recommended to consume fewer fried foods and a more plant-based diet to decrease obesity risk. This result can be applied to personalized nutrition for preventing obesity. Full article

(This article belongs to the Special Issue Nutritional Genomics—Fundamental and Clinical Aspects)

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10 pages, 2257 KiB

Open AccessArticle

Epigenome-Wide Study Identified Methylation Sites Associated with the Risk of Obesity

by Majid Nikpay, Sepehr Ravati, Robert Dent and Ruth McPherson

Nutrients 2021, 13(6), 1984; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13061984 - 09 Jun 2021

Cited by 8 | Viewed by 3026

Abstract

Here, we performed a genome-wide search for methylation sites that contribute to the risk of obesity. We integrated methylation quantitative trait locus (mQTL) data with BMI GWAS information through a SNP-based multiomics approach to identify genomic regions where mQTLs for a methylation site co-localize with obesity risk SNPs. We then tested whether the identified site contributed to BMI through Mendelian randomization. We identified multiple methylation sites causally contributing to the risk of obesity. We validated these findings through a replication stage. By integrating expression quantitative trait locus (eQTL) data, we noted that lower methylation at cg21178254 site upstream of CCNL1 contributes to obesity by increasing the expression of this gene. Higher methylation at cg02814054 increases the risk of obesity by lowering the expression of MAST3, whereas lower methylation at cg06028605 contributes to obesity by decreasing the expression of SLC5A11. Finally, we noted that rare variants within 2p23.3 impact obesity by making the cg01884057 site more susceptible to methylation, which consequently lowers the expression of POMC, ADCY3 and DNAJC27. In this study, we identify methylation sites associated with the risk of obesity and reveal the mechanism whereby a number of these sites exert their effects. This study provides a framework to perform an omics-wide association study for a phenotype and to understand the mechanism whereby a rare variant causes a disease. Full article

(This article belongs to the Special Issue Nutritional Genomics—Fundamental and Clinical Aspects)

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