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Special Issue "Gene-Diet Interactions in Chronic Diseases"

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

Deadline for manuscript submissions: closed (30 June 2017).

Special Issue Editors

Prof. Dr. Lynnette Ferguson
E-Mail Website
Guest Editor
Discipline of Nutrition and Dietetics, Faculty of Medical and Health Sciences, The University of Auckland, Private Bag 92019, Auckland 1142, New Zealand
Interests: nutrigenetics; nutrigenomics; nutrigenomics technologies; genetic toxicology; DNA damage and repair; environmental mutagenesis; environmental carcinogenesis; mechanisms of anticancer drug action; gene–diet interactions—particularly in prostate and colorectal cancer; inflammatory bowel disease and other inflammation-related disorders
Special Issues, Collections and Topics in MDPI journals
Ms. Virginia R. Parslow
E-Mail
Guest Editor
Faculty of Medical and Health Science, University of Auckland, Private Bag 92019, Auckland 1142, New Zealand
Interests: nutritional intervention; systems biology; integrative medicine; gene-diet interactions; personalised nutrition

Special Issue Information

Dear Colleagues,

Three main factors have contributed to the emergence of nutrigenetics: The sequencing of the human, mouse and rat genomes, new understandings of the ways in which macronutrients and micronutrients interact with our genetic makeup, and improved understanding of the mechanisms that underlie chronic inflammation—a central factor in many common diseases, particularly those of a chronic nature.

Among omics tools available, transcriptomics, proteomics and metabolomics have, together, produced molecular biomarkers that allow early dietary intervention which can reverse the onset of diet-related diseases and help regain homeostasis. Microbiomics is also growing as an important tool that studies the genome of a person’s microbiota and enables study of interactions between host’s genome and microbiome plus environmental factors, particularly diet.

Chronic inflammation is understood to be a common underlying mechanism of several chronic diseases, including cardiovascular disease, diabetes, cancer, inflammatory bowel disease, Alzheimer’s disease, asthma, and rheumatoid arthritis. The interplay between genes and diet in the development of chronic disease has been well-documented in recent years, with some studies showing that intervening “upstream” with nutrient intervention can positively impact lower-grade chronic conditions developing into more serious status.

Nutrigenetics has developed at a pace that is often ahead of regulatory guidelines, and outside of practitioner and public understanding. This has not prevented motivated, tech-savvy consumers and patients from accessing genetic and nutritional information, which they see as ‘rightly theirs to know and apply as they wish’. Furthermore, there have been numerous examples that support the usefulness of this tool.  Given that those with chronic disease or a predisposition to such are often more motivated than others to learn ways in which to help themselves, personalised nutrition is of particular interest.

This Special Issue, “Gene-Diet Interactions in Chronic Diseases”, will focus on the role of nutrigenetics and the application of personalised nutrition in chronic disease. Experimental papers, up-to-date review articles, and commentaries are all welcome.

Prof. Dr. Lynnette R. Ferguson
Ms. Virginia R. Parslow
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • nutrigenetics
  • nutrigenomics
  • personalised nutrition
  • chronic disease
  • inflammation
  • gene-diet interaction
  • environment
  • omics technologies

Published Papers (9 papers)

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Research

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Article
Suppression of Ghrelin Exacerbates HFCS-Induced Adiposity and Insulin Resistance
Int. J. Mol. Sci. 2017, 18(6), 1302; https://doi.org/10.3390/ijms18061302 - 19 Jun 2017
Cited by 13 | Viewed by 2742
Abstract
High fructose corn syrup (HFCS) is widely used as sweetener in processed foods and soft drinks in the United States, largely substituting sucrose (SUC). The orexigenic hormone ghrelin promotes obesity and insulin resistance; ghrelin responds differently to HFCS and SUC ingestion. Here we [...] Read more.
High fructose corn syrup (HFCS) is widely used as sweetener in processed foods and soft drinks in the United States, largely substituting sucrose (SUC). The orexigenic hormone ghrelin promotes obesity and insulin resistance; ghrelin responds differently to HFCS and SUC ingestion. Here we investigated the roles of ghrelin in HFCS- and SUC-induced adiposity and insulin resistance. To mimic soft drinks, 10-week-old male wild-type (WT) and ghrelin knockout (Ghrelin−/−) mice were subjected to ad lib. regular chow diet supplemented with either water (RD), 8% HFCS (HFCS), or 10% sucrose (SUC). We found that SUC-feeding induced more robust increases in body weight and body fat than HFCS-feeding. Comparing to SUC-fed mice, HFCS-fed mice showed lower body weight but higher circulating glucose and insulin levels. Interestingly, we also found that ghrelin deletion exacerbates HFCS-induced adiposity and inflammation in adipose tissues, as well as whole-body insulin resistance. Our findings suggest that HFCS and SUC have differential effects on lipid metabolism: while sucrose promotes obesogenesis, HFCS primarily enhances inflammation and insulin resistance, and ghrelin confers protective effects for these metabolic dysfunctions. Full article
(This article belongs to the Special Issue Gene-Diet Interactions in Chronic Diseases)
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Article
Metabolic Effect of an Oriental Herbal Medicine on Obesity and Its Comorbidities with Transcriptional Responses in Diet-Induced Obese Mice
Int. J. Mol. Sci. 2017, 18(4), 747; https://doi.org/10.3390/ijms18040747 - 01 Apr 2017
Cited by 3 | Viewed by 2418
Abstract
Taeeumjowuitang (TJ) is an alternative herbal medicine that has been used to treat obesity in Korea. The molecular mechanisms involved in TJ-induced anti-obesity effects have not yet been determined. The aim of the current study was to elucidate the effects of TJ on [...] Read more.
Taeeumjowuitang (TJ) is an alternative herbal medicine that has been used to treat obesity in Korea. The molecular mechanisms involved in TJ-induced anti-obesity effects have not yet been determined. The aim of the current study was to elucidate the effects of TJ on obesity and metabolic syndrome, by analyzing the transcriptional and metabolic responses to TJ treatment. C57BL/6J mice were fed a high-fat or high-fat + 3% (w/w) TJ diet for 12 weeks. Their phenotypic characteristics were measured and the anti-obesity mechanism was elucidated, based on the RNA sequencing (RNA-seq) transcriptomic profiles in an animal model of obesity. TJ treatment ameliorated insulin resistance, dyslipidemia, and hepatic steatosis in high-fat diet-induced obese mice, with a simultaneous reduction in body weight gain by enhancing energy expenditure and suppressing adiposity. An analysis of the global transcriptional changes by RNA-seq revealed that TJ upregulated mitochondrial oxidative phosphorylation-associated genes in epididymal white adipose tissue (eWAT), suggesting an enhanced mitochondrial function after TJ treatment. Moreover, TJ effectively attenuated the high-fat diet-induced inflammatory response through transcriptional changes in eWAT. Our findings provide some mechanistic insights into the effects of TJ, an alternative oriental medicine, in the treatment of obesity and its comorbidities. They demonstrate that metabolic and transcriptional responses to diet-induced obesity with TJ treatment were desirable in adipose tissue metabolism. Full article
(This article belongs to the Special Issue Gene-Diet Interactions in Chronic Diseases)
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Article
Plasma Triglyceride Levels May Be Modulated by Gene Expression of IQCJ, NXPH1, PHF17 and MYB in Humans
Int. J. Mol. Sci. 2017, 18(2), 257; https://doi.org/10.3390/ijms18020257 - 26 Jan 2017
Cited by 9 | Viewed by 2203
Abstract
A genome-wide association study (GWAS) by our group identified loci associated with the plasma triglyceride (TG) response to ω-3 fatty acid (FA) supplementation in IQCJ, NXPH1, PHF17 and MYB. Our aim is to investigate potential mechanisms underlying the associations between [...] Read more.
A genome-wide association study (GWAS) by our group identified loci associated with the plasma triglyceride (TG) response to ω-3 fatty acid (FA) supplementation in IQCJ, NXPH1, PHF17 and MYB. Our aim is to investigate potential mechanisms underlying the associations between single nucleotide polymorphisms (SNPs) in the four genes and TG levels following ω-3 FA supplementation. 208 subjects received 3 g/day of ω-3 FA (1.9–2.2 g of EPA and 1.1 g of docosahexaenoic acid (DHA)) for six weeks. Plasma TG were measured before and after the intervention. 67 SNPs were selected to increase the density of markers near GWAS hits. Genome-wide expression and methylation analyses were conducted on respectively 30 and 35 participants’ blood sample together with in silico analyses. Two SNPs of IQCJ showed different affinities to splice sites depending on alleles. Expression levels were influenced by genotype for one SNP in NXPH1 and one in MYB. Associations between 12 tagged SNPs of IQCJ, 26 of NXPH1, seven of PHF17 and four of MYB and gene-specific CpG site methylation levels were found. The response of plasma TG to ω-3 FA supplementation may be modulated by the effect of DNA methylation on expression levels of genes revealed by GWAS. Full article
(This article belongs to the Special Issue Gene-Diet Interactions in Chronic Diseases)
Article
Troxerutin Attenuates Enhancement of Hepatic Gluconeogenesis by Inhibiting NOD Activation-Mediated Inflammation in High-Fat Diet-Treated Mice
Int. J. Mol. Sci. 2017, 18(1), 31; https://doi.org/10.3390/ijms18010031 - 25 Dec 2016
Cited by 24 | Viewed by 3728
Abstract
Recent evidence suggests that troxerutin, a trihydroxyethylated derivative of natural bioflavonoid rutin, exhibits beneficial effects on diabetes-related symptoms. Here we investigated the effects of troxerutin on the enhancement of hepatic gluconeogenesis in high-fat diet (HFD)-treated mice and the mechanisms underlying these effects. Mice [...] Read more.
Recent evidence suggests that troxerutin, a trihydroxyethylated derivative of natural bioflavonoid rutin, exhibits beneficial effects on diabetes-related symptoms. Here we investigated the effects of troxerutin on the enhancement of hepatic gluconeogenesis in high-fat diet (HFD)-treated mice and the mechanisms underlying these effects. Mice were divided into four groups: Control group, HFD group, HFD + Troxerutin group, and Troxerutin group. Troxerutin was treated by daily oral administration at doses of 150 mg/kg/day for 20 weeks. Tauroursodeoxycholic acid (TUDCA) was used to inhibit endoplasmic reticulum stress (ER stress). Our results showed that troxerutin effectively improved obesity and related metabolic parameters, and liver injuries in HFD-treated mouse. Furthermore, troxerutin significantly attenuated enhancement of hepatic gluconeogenesis in HFD-fed mouse. Moreover, troxerutin notably suppressed nuclear factor-κB (NF-κB) p65 transcriptional activation and release of inflammatory cytokines in HFD-treated mouse livers. Mechanismly, troxerutin dramatically decreased Nucleotide oligomerization domain (NOD) expression, as well as interaction between NOD1/2 with interacting protein-2 (RIP2), by abating oxidative stress-induced ER stress in HFD-treated mouse livers, which was confirmed by TUDCA treatment. These improvement effects of troxerutin on hepatic glucose disorders might be mediated by its anti-obesity effect. In conclusion, troxerutin markedly diminished HFD-induced enhancement of hepatic gluconeogenesis via its inhibitory effects on ER stress-mediated NOD activation and consequent inflammation, which might be mediated by its anti-obesity effect. Full article
(This article belongs to the Special Issue Gene-Diet Interactions in Chronic Diseases)
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Review

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Review
Gene-Diet Interactions in Type 2 Diabetes: The Chicken and Egg Debate
Int. J. Mol. Sci. 2017, 18(6), 1188; https://doi.org/10.3390/ijms18061188 - 02 Jun 2017
Cited by 35 | Viewed by 4964
Abstract
Consistent evidence from both experimental and human studies indicates that Type 2 diabetes mellitus (T2DM) is a complex disease resulting from the interaction of genetic, epigenetic, environmental, and lifestyle factors. Nutrients and dietary patterns are important environmental factors to consider in the prevention, [...] Read more.
Consistent evidence from both experimental and human studies indicates that Type 2 diabetes mellitus (T2DM) is a complex disease resulting from the interaction of genetic, epigenetic, environmental, and lifestyle factors. Nutrients and dietary patterns are important environmental factors to consider in the prevention, development and treatment of this disease. Nutritional genomics focuses on the interaction between bioactive food components and the genome and includes studies of nutrigenetics, nutrigenomics and epigenetic modifications caused by nutrients. There is evidence supporting the existence of nutrient-gene and T2DM interactions coming from animal studies and family-based intervention studies. Moreover, many case-control, cohort, cross-sectional cohort studies and clinical trials have identified relationships between individual genetic load, diet and T2DM. Some of these studies were on a large scale. In addition, studies with animal models and human observational studies, in different countries over periods of time, support a causative relationship between adverse nutritional conditions during in utero development, persistent epigenetic changes and T2DM. This review provides comprehensive information on the current state of nutrient-gene interactions and their role in T2DM pathogenesis, the relationship between individual genetic load and diet, and the importance of epigenetic factors in influencing gene expression and defining the individual risk of T2DM. Full article
(This article belongs to the Special Issue Gene-Diet Interactions in Chronic Diseases)
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Review
Molecular Basis of Alcohol-Related Gastric and Colon Cancer
Int. J. Mol. Sci. 2017, 18(6), 1116; https://doi.org/10.3390/ijms18061116 - 24 May 2017
Cited by 53 | Viewed by 5286
Abstract
Many meta-analysis, large cohort studies, and experimental studies suggest that chronic alcohol consumption increases the risk of gastric and colon cancer. Ethanol is metabolized by alcohol dehydrogenases (ADH), catalase or cytochrome P450 2E1 (CYP2E1) to acetaldehyde, which is then further oxidized to acetate [...] Read more.
Many meta-analysis, large cohort studies, and experimental studies suggest that chronic alcohol consumption increases the risk of gastric and colon cancer. Ethanol is metabolized by alcohol dehydrogenases (ADH), catalase or cytochrome P450 2E1 (CYP2E1) to acetaldehyde, which is then further oxidized to acetate by aldehyde dehydrogenase (ALDH). Acetaldehyde has been classified by the International Agency for Research on Cancer (IARC) as a Group 1 carcinogen to humans. The acetaldehyde level in the stomach and colon is locally influenced by gastric colonization by Helicobacter pylori or colonic microbes, as well as polymorphisms in the genes encoding tissue alcohol metabolizing enzymes, especially ALDH2. Alcohol stimulates the uptake of carcinogens and their metabolism and also changes the composition of enteric microbes in a way to enhance the aldehyde level. Alcohol also undergoes chemical coupling to membrane phospholipids and disrupts organization of tight junctions, leading to nuclear translocation of β-catenin and ZONAB, which may contributes to regulation of genes involved in proliferation, invasion and metastasis. Alcohol also generates reactive oxygen species (ROS) by suppressing the expression of antioxidant and cytoprotective enzymes and inducing expression of CYP2E1 which contribute to the metabolic activation of chemical carcinogens. Besides exerting genotoxic effects by directly damaging DNA, ROS can activates signaling molecules involved in inflammation, metastasis and angiogenesis. In addition, alcohol consumption induces folate deficiency, which may result in aberrant DNA methylation profiles, thereby influencing cancer-related gene expression. Full article
(This article belongs to the Special Issue Gene-Diet Interactions in Chronic Diseases)
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Review
NutrimiRAging: Micromanaging Nutrient Sensing Pathways through Nutrition to Promote Healthy Aging
Int. J. Mol. Sci. 2017, 18(5), 915; https://doi.org/10.3390/ijms18050915 - 26 Apr 2017
Cited by 14 | Viewed by 3659
Abstract
Current sociodemographic predictions point to a demographic shift in developed and developing countries that will result in an unprecedented increase of the elderly population. This will be accompanied by an increase in age-related conditions that will strongly impair human health and quality of [...] Read more.
Current sociodemographic predictions point to a demographic shift in developed and developing countries that will result in an unprecedented increase of the elderly population. This will be accompanied by an increase in age-related conditions that will strongly impair human health and quality of life. For this reason, aging is a major concern worldwide. Healthy aging depends on a combination of individual genetic factors and external environmental factors. Diet has been proved to be a powerful tool to modulate aging and caloric restriction has emerged as a valuable intervention in this regard. However, many questions about how a controlled caloric restriction intervention affects aging-related processes are still unanswered. Nutrient sensing pathways become deregulated with age and lose effectiveness with age. These pathways are a link between diet and aging. Thus, fully understanding this link is a mandatory step before bringing caloric restriction into practice. MicroRNAs have emerged as important regulators of cellular functions and can be modified by diet. Some microRNAs target genes encoding proteins and enzymes belonging to the nutrient sensing pathways and, therefore, may play key roles in the modulation of the aging process. In this review, we aimed to show the relationship between diet, nutrient sensing pathways and microRNAs in the context of aging. Full article
(This article belongs to the Special Issue Gene-Diet Interactions in Chronic Diseases)
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Review
Skeletal Muscle Nucleo-Mitochondrial Crosstalk in Obesity and Type 2 Diabetes
Int. J. Mol. Sci. 2017, 18(4), 831; https://doi.org/10.3390/ijms18040831 - 14 Apr 2017
Cited by 24 | Viewed by 3688
Abstract
Skeletal muscle mitochondrial dysfunction, evidenced by incomplete beta oxidation and accumulation of fatty acid intermediates in the form of long and medium chain acylcarnitines, may contribute to ectopic lipid deposition and insulin resistance during high fat diet (HFD)-induced obesity. The present review discusses [...] Read more.
Skeletal muscle mitochondrial dysfunction, evidenced by incomplete beta oxidation and accumulation of fatty acid intermediates in the form of long and medium chain acylcarnitines, may contribute to ectopic lipid deposition and insulin resistance during high fat diet (HFD)-induced obesity. The present review discusses the roles of anterograde and retrograde communication in nucleo-mitochondrial crosstalk that determines skeletal muscle mitochondrial adaptations, specifically alterations in mitochondrial number and function in relation to obesity and insulin resistance. Special emphasis is placed on the effects of high fat diet (HFD) feeding on expression of nuclear-encoded mitochondrial genes (NEMGs) nuclear receptor factor 1 (NRF-1) and 2 (NRF-2) and peroxisome proliferator receptor gamma coactivator 1 alpha (PGC-1α) in the onset and progression of insulin resistance during obesity and how HFD-induced alterations in NEMG expression affect skeletal muscle mitochondrial adaptations in relation to beta oxidation of fatty acids. Finally, the potential ability of acylcarnitines or fatty acid intermediates resulting from mitochondrial beta oxidation to act as retrograde signals in nucleo-mitochondrial crosstalk is reviewed and discussed. Full article
(This article belongs to the Special Issue Gene-Diet Interactions in Chronic Diseases)
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Review
Gene-Diet Interaction and Precision Nutrition in Obesity
Int. J. Mol. Sci. 2017, 18(4), 787; https://doi.org/10.3390/ijms18040787 - 07 Apr 2017
Cited by 74 | Viewed by 9613
Abstract
The rapid rise of obesity during the past decades has coincided with a profound shift of our living environment, including unhealthy dietary patterns, a sedentary lifestyle, and physical inactivity. Genetic predisposition to obesity may have interacted with such an obesogenic environment in determining [...] Read more.
The rapid rise of obesity during the past decades has coincided with a profound shift of our living environment, including unhealthy dietary patterns, a sedentary lifestyle, and physical inactivity. Genetic predisposition to obesity may have interacted with such an obesogenic environment in determining the obesity epidemic. Growing studies have found that changes in adiposity and metabolic response to low-calorie weight loss diets might be modified by genetic variants related to obesity, metabolic status and preference to nutrients. This review summarized data from recent studies of gene-diet interactions, and discussed integration of research of metabolomics and gut microbiome, as well as potential application of the findings in precision nutrition. Full article
(This article belongs to the Special Issue Gene-Diet Interactions in Chronic Diseases)
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