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Nutrigenomics in Health and Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (31 July 2021) | Viewed by 35484

Special Issue Editors

Department of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy
Interests: medical genetics; molecular genetics; coagulation; hemorrhagic and thrombotic diseases; hereditary angioedema
Department of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy
Interests: healthy aging; nutrition; exercise; disease prevention; lifestyle interventions; metabolic health; cognitive function; physical performance
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Nutrigenomics is a new discipline attempting to understand the effects of food on multiple molecular levels, such as genomics and epigenomics. Lifestyle changes, such as the use of personalized diets, increased physical activity, and, consecutively, weight loss, can have a beneficial effect on the epigenome and, thus, on the risk of suffering a number of diseases based on metabolic impairment.
The purpose of this Special Issue is to provide an overview of the principles of nutrigenomics and the interrelationships of diet, genomics, and health outcomes, with a focus on chronic disease endpoints.

Topics of interest for this Special Issue include the following:

  • “Molecular genetic basis" and the "links to disease" that look at nutrigenomics from the perspective of molecular mechanisms or the causes of metabolic diseases, respectively.
  • The genome influences upon pharmacological and diet treatments.
  • The impact of polymorphism in terms of personalized recommendations.
  • The role played by the microbiome in personalized nutrition.
  • Mitochondrial genetics and its relationship with disease risk.
  • The role of both precision medicine and precision nutrition as a paradigm to develop targeted interventions.

Prof. Dr. Maurizio Margaglione
Prof. Dr. Giuseppe Cibelli
Guest Editors

Manuscript Submission Information

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Keywords

  • polimorphism;
  • obesity;
  • precision nutrition;
  • dietary efficacy;
  • Genetic variation;
  • Metabolomics;
  • Microbiome;

Published Papers (4 papers)

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Research

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12 pages, 1659 KiB  
Article
Diet-Related Alterations of Gut Bile Salt Hydrolases Determined Using a Metagenomic Analysis of the Human Microbiome
by Baolei Jia, Dongbin Park, Byung Hee Chun, Yoonsoo Hahn and Che Ok Jeon
Int. J. Mol. Sci. 2021, 22(7), 3652; https://doi.org/10.3390/ijms22073652 - 01 Apr 2021
Cited by 15 | Viewed by 3226
Abstract
The metabolism of bile acid by the gut microbiota is associated with host health. Bile salt hydrolases (BSHs) play a crucial role in controlling microbial bile acid metabolism. Herein, we conducted a comparative study to investigate the alterations in the abundance of BSHs [...] Read more.
The metabolism of bile acid by the gut microbiota is associated with host health. Bile salt hydrolases (BSHs) play a crucial role in controlling microbial bile acid metabolism. Herein, we conducted a comparative study to investigate the alterations in the abundance of BSHs using data from three human studies involving dietary interventions, which included a ketogenetic diet (KD) versus baseline diet (BD), overfeeding diet (OFD) versus underfeeding diet, and low-carbohydrate diet (LCD) versus BD. The KD increased BSH abundance compared to the BD, while the OFD and LCD did not change the total abundance of BSHs in the human gut. BSHs can be classified into seven clusters; Clusters 1 to 4 are relatively abundant in the gut. In the KD cohort, the levels of BSHs from Clusters 1, 3, and 4 increased significantly, whereas there was no notable change in the levels of BSHs from the clusters in the OFD and LCD cohorts. Taxonomic studies showed that members of the phyla Bacteroidetes, Firmicutes, and Actinobacteria predominantly produced BSHs. The KD altered the community structure of BSH-active bacteria, causing an increase in the abundance of Bacteroidetes and decrease in Actinobacteria. In contrast, the abundance of BSH-active Bacteroidetes decreased in the OFD cohort, and no significant change was observed in the LCD cohort. These results highlight that dietary patterns are associated with the abundance of BSHs and community structure of BSH-active bacteria and demonstrate the possibility of manipulating the composition of BSHs in the gut through dietary interventions to impact human health. Full article
(This article belongs to the Special Issue Nutrigenomics in Health and Diseases)
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14 pages, 1759 KiB  
Article
IFNγ Is a Key Link between Obesity and Th1-Mediated AutoImmune Diseases
by Heekyong R. Bae, Myung-Sook Choi, Suntae Kim, Howard A. Young, M. Eric Gershwin, Seon-Min Jeon and Eun-Young Kwon
Int. J. Mol. Sci. 2021, 22(1), 208; https://doi.org/10.3390/ijms22010208 - 28 Dec 2020
Cited by 10 | Viewed by 2861
Abstract
Obesity, a characteristic of metabolic syndrome, is also associated with chronic inflammation and the development of autoimmune diseases. However, the relationship between obesity and autoimmune diseases remains to be investigated in depth. Here, we compared hepatic gene expression profiles among high-fat diet (HFD) [...] Read more.
Obesity, a characteristic of metabolic syndrome, is also associated with chronic inflammation and the development of autoimmune diseases. However, the relationship between obesity and autoimmune diseases remains to be investigated in depth. Here, we compared hepatic gene expression profiles among high-fat diet (HFD) mice using the primary biliary cholangitis (PBC) mouse model based on the chronic expression of interferon gamma (IFNγ) (ARE-Del-/- mice). The top differentially expressed genes affected by upstream transcriptional regulators IFNγ, LPS, and TNFα displayed an overlap in HFD and ARE-Del-/- mice, indicating that obesity-induced liver inflammation may be dependent on signaling via IFNγ. The top pathways altered in HFD mice were mostly involved in the innate immune responses, which overlapped with ARE-Del-/- mice. In contrast, T cell-mediated signaling pathways were exclusively altered in ARE-Del-/- mice. We further evaluated the therapeutic effect of luteolin, known as anti-inflammatory flavonoid, in HFD and ARE-Del-/- mice. Luteolin strongly suppressed the MHC I and II antigen presentation pathways, which were highly activated in both HFD and ARE-Del-/- mice. Conversely, luteolin increased metabolic processes of fatty acid oxidation and oxidative phosphorylation in the liver, which were suppressed in ARE-Del-/- mice. Luteolin also strongly induced PPAR signaling, which was downregulated in HFD and ARE-Del-/- mice. Using human GWAS data, we characterized the genetic interaction between significant obesity-related genes and IFNγ signaling and demonstrated that IFNγ is crucial for obesity-mediated inflammatory responses. Collectively, this study improves our mechanistic understanding of the relationship between obesity and autoimmune diseases. Furthermore, it provides new methodological insights into how immune network-based analyses effectively integrate RNA-seq and microarray data. Full article
(This article belongs to the Special Issue Nutrigenomics in Health and Diseases)
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Review

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24 pages, 1117 KiB  
Review
Association of Vitamin D Metabolism Gene Polymorphisms with Autoimmunity: Evidence in Population Genetic Studies
by Adolfo I. Ruiz-Ballesteros, Mónica R. Meza-Meza, Barbara Vizmanos-Lamotte, Isela Parra-Rojas and Ulises de la Cruz-Mosso
Int. J. Mol. Sci. 2020, 21(24), 9626; https://doi.org/10.3390/ijms21249626 - 17 Dec 2020
Cited by 47 | Viewed by 9336
Abstract
A high prevalence of vitamin D (calcidiol) serum deficiency has been described in several autoimmune diseases, including multiple sclerosis (MS), rheumatoid arthritis (AR), and systemic lupus erythematosus (SLE). Vitamin D is a potent immunonutrient that through its main metabolite calcitriol, regulates the immunomodulation [...] Read more.
A high prevalence of vitamin D (calcidiol) serum deficiency has been described in several autoimmune diseases, including multiple sclerosis (MS), rheumatoid arthritis (AR), and systemic lupus erythematosus (SLE). Vitamin D is a potent immunonutrient that through its main metabolite calcitriol, regulates the immunomodulation of macrophages, dendritic cells, T and B lymphocytes, which express the vitamin D receptor (VDR), and they produce and respond to calcitriol. Genetic association studies have shown that up to 65% of vitamin D serum variance may be explained due to genetic background. The 90% of genetic variability takes place in the form of single nucleotide polymorphisms (SNPs), and SNPs in genes related to vitamin D metabolism have been linked to influence the calcidiol serum levels, such as in the vitamin D binding protein (VDBP; rs2282679 GC), 25-hydroxylase (rs10751657 CYP2R1), 1α-hydroxylase (rs10877012, CYP27B1) and the vitamin D receptor (FokI (rs2228570), BsmI (rs1544410), ApaI (rs7975232), and TaqI (rs731236) VDR). Therefore, the aim of this comprehensive literature review was to discuss the current findings of functional SNPs in GC, CYP2R1, CYP27B1, and VDR associated to genetic risk, and the most common clinical features of MS, RA, and SLE. Full article
(This article belongs to the Special Issue Nutrigenomics in Health and Diseases)
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20 pages, 783 KiB  
Review
Various Aspects of a Gene Editing System—CRISPR–Cas9
by Edyta Janik, Marcin Niemcewicz, Michal Ceremuga, Lukasz Krzowski, Joanna Saluk-Bijak and Michal Bijak
Int. J. Mol. Sci. 2020, 21(24), 9604; https://doi.org/10.3390/ijms21249604 - 16 Dec 2020
Cited by 55 | Viewed by 19114
Abstract
The discovery of clustered, regularly interspaced short palindromic repeats (CRISPR) and their cooperation with CRISPR-associated (Cas) genes is one of the greatest advances of the century and has marked their application as a powerful genome engineering tool. The CRISPR–Cas system was discovered as [...] Read more.
The discovery of clustered, regularly interspaced short palindromic repeats (CRISPR) and their cooperation with CRISPR-associated (Cas) genes is one of the greatest advances of the century and has marked their application as a powerful genome engineering tool. The CRISPR–Cas system was discovered as a part of the adaptive immune system in bacteria and archaea to defend from plasmids and phages. CRISPR has been found to be an advanced alternative to zinc-finger nucleases (ZFN) and transcription activator-like effector nucleases (TALEN) for gene editing and regulation, as the CRISPR–Cas9 protein remains the same for various gene targets and just a short guide RNA sequence needs to be altered to redirect the site-specific cleavage. Due to its high efficiency and precision, the Cas9 protein derived from the type II CRISPR system has been found to have applications in many fields of science. Although CRISPR–Cas9 allows easy genome editing and has a number of benefits, we should not ignore the important ethical and biosafety issues. Moreover, any tool that has great potential and offers significant capabilities carries a level of risk of being used for non-legal purposes. In this review, we present a brief history and mechanism of the CRISPR–Cas9 system. We also describe on the applications of this technology in gene regulation and genome editing; the treatment of cancer and other diseases; and limitations and concerns of the use of CRISPR–Cas9. Full article
(This article belongs to the Special Issue Nutrigenomics in Health and Diseases)
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