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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 (20 November 2022) | Viewed by 10041

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Dr. Marica Cariello

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Clinica Medica Cesare Frugoni, Department of Interdisciplinary Medicine, University of Bari “Aldo Moro”, 70124 Bari, Italy
Interests: nutrients; nuclear receptors; gut–liver axis; tumorigenesis; cholesterol and lipid metabolism
Special Issues, Collections and Topics in MDPI journals

Dr. Raffaella Maria Gadaleta

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Co-Guest Editor

Clinica Medica Cesare Frugoni, Department of Interdisciplinary Medicine, University of Bari “Aldo Moro”, 70124 Bari, Italy
Interests: nutrition; nutrigenomics; pathophysiology of the gut–liver axis; gastrointestinal; Mediterranean diet
Special Issues, Collections and Topics in MDPI journals

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Dear Colleagues,

Individualized nutrition based on nutrigenomic knowledge is becoming an important area of scientific and health interest. The development of “omics” technologies promotes the individualized nutrition and characterizes the subjects with a personalized approach. Nutrition and lifestyle are crucial factors in the interactions between environment and genes for reaching a healthy status. Personalized nutrition should be based on the principle that food or nutrients may be either risk or defense factors to prevent and manage several diseases, thanks to their ability to regulate gene expression (nutrigenomics). Lipids and glucose are two major energy sources of the organism. Dietary fats are necessary for membrane constitution and act as a precursor for important molecules, such as bile acids and hormones. The accumulation of visceral fat is able to drive inflammation and the modulation of tumoral microenvironment that has a key role in the development and progression of several pathologies such as cancer. Therefore, nutritional programs, lifestyle changes, and prevention are necessary to reduce the incidence of diseases and to improve response to therapy.

We invite authors to submit original research articles, reviews, mini-reviews, or perspectives that address any aspect of nutrigenomic and metabolism in normal and/or pathological conditions.

Dr. Marica Cariello
Dr. Raffaella Maria Gadaleta
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 submissions that pass pre-check are 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 semimonthly 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 2900 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

lipid metabolism
cholesterol metabolism
nutrigenomics
dietary fat
energy intake
diet quality
visceral fat
obesity
personalized nutrition

Published Papers (4 papers)

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Research

19 pages, 1647 KiB

Open AccessArticle

Association of Plant-Based and High-Protein Diets with a Lower Obesity Risk Defined by Fat Mass in Middle-Aged and Elderly Persons with a High Genetic Risk of Obesity

by James W. Daily and Sunmin Park

Nutrients 2023, 15(4), 1063; https://doi.org/10.3390/nu15041063 - 20 Feb 2023

Cited by 2 | Viewed by 3202

Abstract

Obesity has become a severe public health challenge globally. The present study aimed to identify separate and interactive dietary, genetic, and other factors that increase the risk of obesity as measured by body fat (BF) mass. We utilized a genome-wide association study to identify genetic variants associated with high fat mass (obesity; n = 10,502) and combined them to generate polygenic risk scores (PRS) of genetic variants interacting with each other in adults aged over 40 while excluding body-fat-related diseases in a city-hospital-based cohort (n = 53,828). It was validated in Ansan/Ansung plus rural cohorts (n = 13,007). We then evaluated dietary and lifestyle factors in subjects to assess what factors might help overcome a genetic propensity for higher BF. The three-SNP model included brain-derived neurotrophic factor (BDNF)_rs6265, fat-mass- and obesity-associated protein (FTO)_rs1421085, and SEC16B_rs509325. The genes with the minor alleles of ADCY3_rs6545790 and BAIAP2_rs35867081 increased their gene expression in the visceral and subcutaneous adipocytes, but their gene expression decreased in the hypothalamus in eQTL analysis. In the three-SNP model, the PRS was associated with BF mass by 1.408 and 1.396 times after adjusting covariates 1 (age, gender, survey year, residence area, education, and income) and 2 (covariates in model 1 plus energy intake, alcohol intake, regular exercise, and smoking status), respectively. However, when separating subjects by PRS of the three-SNP model, a plant-based diet was the most significant factor associated with low BF, followed by high-protein diets and lower energy intakes. They could offset the effects of high genetic risk for high BF. In conclusion, modulating nutrient intakes might overcome a high genetic risk for obesity. Dietary choices favoring more plant-based and higher-protein foods might help prevent increased BF in Asians and potentially people of other ethnicities with high polygenetic risk scores. Full article

(This article belongs to the Special Issue Nutrigenomic and Metabolism)

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18 pages, 3330 KiB

Open AccessArticle

Association of Polygenic Variants Involved in Immunity and Inflammation with Duodenal Ulcer Risk and Their Interaction with Irregular Eating Habits

by Sunmin Park, Meiling Liu and Shaokai Huang

Nutrients 2023, 15(2), 296; https://doi.org/10.3390/nu15020296 - 06 Jan 2023

Cited by 3 | Viewed by 2060

Abstract

Genetic and environmental factors are associated with developing and progressing duodenal ulcer (DU) risk. However, the exact nature of the disease pathophysiology and the single nucleotide polymorphism (SNP)—lifestyle interaction has yet to be determined. The purpose of the present study was to examine the SNPs linked to DU risk and their interaction with lifestyles and diets in a large hospital-based cohort of Asians. Based on an earlier diagnosis, the participants were divided into the DU (case; n = 1088) and non-DU (control, n = 56,713) groups. The SNP associated with DU risk were obtained from a genome-wide association study (GWAS), and those promoted genetic impact with SNP–SNP interactions were identified with generalized multifactor dimensionality reduction analysis. The interaction between polygenic risk score (PRS) calculated from the selected genetic variants and nutrient were examined. They were related to actin modification, immune response, and cell migration by modulating leucine-rich repeats (LRR) domain binding, Shaffer interferon regulatory factor 4 (IRF4) targets in myeloma vs. mature B lymphocyte, and Reactome runt-related transcription factor 3 (RUNX3). Among the selected SNPs, rs11230563 (R225W) showed missense mutation and low binding affinity with different food components in the autodock analysis. Glycyrrhizin, physalin B, janthitrem F, and casuarinin lowered it in only wild CD6 protein but not in mutated CD6. Plastoquinone 8, solamargine, saponin D, and matesaponin 2 decreased energy binding affinity in mutated CD6 proteins. The PRS of the 5-SNP and 6-SNP models exhibited a positive association with DU risk (OR = 3.14). The PRS of the 5-SNP PRS model interacted with irregular eating habits and smoking status. In participants with irregular eating habits or smokers, DU incidence was much higher in the participants with high PRS than in those with low PRS. In conclusion, the genetic impact of DU risk was mainly in regulating immunity, inflammation, and actin modification. Adults who are genetically susceptible to DU need to eat regularly and to be non-smokers. The results could be applied to personalize nutrition. Full article

(This article belongs to the Special Issue Nutrigenomic and Metabolism)

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10 pages, 290 KiB

Open AccessArticle

The Genetic Variability of Members of the SLC38 Family of Amino Acid Transporters (SLC38A3, SLC38A7 and SLC38A9) Affects Susceptibility to Type 2 Diabetes and Vascular Complications

by Paolina Crocco, Serena Dato, Alberto Montesanto, Anna Rita Bonfigli, Roberto Testa, Fabiola Olivieri, Giuseppe Passarino and Giuseppina Rose

Nutrients 2022, 14(21), 4440; https://doi.org/10.3390/nu14214440 - 22 Oct 2022

Cited by 1 | Viewed by 1612

Abstract

Type 2 Diabetes (T2D) is a metabolic disease associated with long-term complications, with a multifactorial pathogenesis related to the interplay between genetic and modifiable risk factors, of which nutrition is the most relevant. In particular, the importance of proteins and constitutive amino acids (AAs) in disease susceptibility is emerging. The ability to sense and respond to changes in AA supplies is mediated by complex networks, of which AA transporters (AATs) are crucial components acting also as sensors of AA availability. This study explored the associations between polymorphisms in selected AATs genes and T2D and vascular complications in 433 patients and 506 healthy controls. Analyses revealed significant association of SLC38A3-rs1858828 with disease risk. Stratification of patients based on presence/absence of vascular complications highlighted significant associations of SLC7A8-rs3783436 and SLC38A7-rs9806843 with diabetic retinopathy. Additionally, the SLC38A9-rs4865615 resulted associated with chronic kidney disease. Notably, these genes function as AAs sensors, specifically glutamine, leucine, and arginine, linked to the main nutrient signaling pathway mammalian target of rapamycin complex 1 (mTORC1). Thus, their genetic variability may contribute to T2D by influencing the ability to properly transduce a signal activating mTORC1 in response to AA availability. In this scenario, the contribution of dietary AAs supply to disease risk may be relevant. Full article

(This article belongs to the Special Issue Nutrigenomic and Metabolism)

15 pages, 2860 KiB

Open AccessArticle

Orphan Nuclear Receptor RORγ Modulates the Genome-Wide Binding of the Cholesterol Metabolic Genes during Mycotoxin-Induced Liver Injury

by Kaiqi Li, Hao Li, Kexin Zhang, Jinying Zhang, Ping Hu, Yanwei Li, Haotian Gu, Hao-Yu Liu, Zhangping Yang and Demin Cai

Nutrients 2021, 13(8), 2539; https://doi.org/10.3390/nu13082539 - 25 Jul 2021

Cited by 10 | Viewed by 2432

Abstract

Maintaining lipid homeostasis is crucial to liver function, the key organ that governs the whole-body energy metabolism. In contrast, lipid dysregulation has been implicated in mycotoxin-induced liver injury, by which the pathophysiological regulation and the molecular components involved remain elusive. Here we focused on the potential roles of orphan nuclear receptor (NR) RORγ in lipid programming, and aimed to explore its action on cholesterol regulation in the liver of mycotoxin-exposed piglets. We found that liver tissues were damaged in the mycotoxin-exposed piglets compared to the healthy controls, revealed by histological analysis, elevated seral ALT, AST and ALP levels, and increased caspase 3/7 activities. Consistent with the transcriptomic finding of down-regulated cholesterol metabolism, we demonstrated that both cholesterol contents and cholesterol biosynthesis/transformation gene expressions in the mycotoxin-exposed livers were reduced, including HMGCS1, FDPS, SQLE, EBP, FDFT1 and VLDLR. Furthermore, we reported that RORγ binds to the cholesterol metabolic genes in porcine hepatocytes using a genome-wide ChIP-seq analysis, whereas mycotoxin decreased the RORγ binding occupancies genome-wide, especially at the cholesterol metabolic pathway. In addition, we revealed the enrichment of co-factors p300 and SRC, the histone marks H3K27ac and H3K4me2, together with RNA Polymerase II (Pol-II) at the locus of HMGCS1 in hepatocytes, which were reduced by mycotoxin-exposure. Our results provide a deep insight into the cholesterol metabolism regulation during mycotoxin-induced liver injury, and propose NRs as therapeutic targets for anti-mycotoxin treatments. Full article

(This article belongs to the Special Issue Nutrigenomic and Metabolism)

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