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Special Issue "Nutrigenetics and Nutrigenomics"

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A special issue of Nutrients (ISSN 2072-6643).

Deadline for manuscript submissions: closed (31 August 2012)

Special Issue Editor

Guest Editor

Dr. Catherine Phillips (Website)

HRB Centre for Diet and Health Research, Department of Epidemiology and Public Health, University College Cork, Ireland and School of Public Health, Physiotherapy and Sports Science, University College Dublin, Ireland
Fax: +353 01 716 3421
Interests: dietary and lifestyle determinants of metabolically healthy obesity; nutrigenetics; metabolic syndrome; nutritional and genetic epidemiology in the context of maternal; childhood, adult and intergenerational obesity; metabolic health and disease

Special Issue Information

Dear Colleagues,

An individual's phenotype represents a complex interaction between the genetic and environmental factors over their lifetime. Nutrition is a key environmental factor in the pathogenesis and progression of common polygenic, diet-related cardiometabolic diseases such as obesity, metabolic syndrome, diabetes and cardiovascular disease. Nutrigenomics and nutrigenetics are rapidly emerging multidisciplinary sciences, which aim to explore the effects of nutrients on the genome, proteome and metabolome, and to elucidate the effect of genetic variation on the interaction between diet and disease. Nutrigenetics has the potential to change the future of dietary guidelines and diet-related disease prevention and therapy. A personalised nutrition approach based on identification of nutrient sensitive or responsive genotypes, whereby nutrient intake is manipulated or optimised based on an individuals' genetic profile to reduce disease risk or improve effectiveness of dietary recommendations, offers the potential to break the traditional public health "one size fits all" approach.

This special issue will highlight emerging research which contributes to our understanding of the role of nutrigenetics and/or nutrigenomics in the development, prevention and treatment of disease. Both research articles and reviews which explore these topics across a wide spectrum of diseases/phenotypes and research activity; from cellular and animal models, through to human studies and epidemiology are welcome.

Dr. Catherine Phillips
Guest Editor

Keywords

nutrigenetics
nutrigenomics
gene-environment interactions
personalised nutrition
diet
nutrient responsive genotypes
obesity
diabetes
metabolic syndrome
cancer

Published Papers (7 papers)

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Research

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Open AccessArticle Selenium, Selenoprotein Genes and Crohn’s Disease in a Case-Control Population from Auckland, New Zealand

by Liljana Gentschew, Karen S. Bishop, Dug Yeo Han, Angharad R. Morgan, Alan G. Fraser, Wen Jiun Lam, Nishi Karunasinghe, Bobbi Campbell and Lynnette R. Ferguson

Nutrients 2012, 4(9), 1247-1259; doi:10.3390/nu4091247

Received: 13 July 2012 / Revised: 23 August 2012 / Accepted: 27 August 2012 / Published: 7 September 2012

Cited by 10 | PDF Full-text (411 KB) | HTML Full-text | XML Full-text

Abstract

New Zealand has one of the highest incidence rates of Crohn’s Disease (CD), whilst the serum selenium status of New Zealanders is amongst the lowest in the world. A prospective case-control study in Auckland, New Zealand considered serum selenium as a potential CD risk factor. Serum selenium levels were significantly lower in CD patients compared to controls (101.8 ± 1.02 vs. 111.1 ± 1.01 ng/mL) (p = 5.91 × 10⁻⁸). Recent detailed studies in the United Kingdom have suggested an optimal serum level around 122 ng/mL, making the average CD patient in New Zealand selenium deficient. Of the 29 single nucleotide polymorphisms (SNPs) tested, 13 were found to significantly interact with serum selenium on CD. After adjustment for multiple testing, a significant interaction with serum selenium on CD was found for three SNPs, namely rs17529609 and rs7901303 in the gene SEPHS1, and rs1553153 in the gene SEPSECS. These three SNPs have not been reported elsewhere as being significantly associated with selenium or CD. It is unclear as to whether lower selenium levels are a cause or an effect of the disease. Full article

(This article belongs to the Special Issue Nutrigenetics and Nutrigenomics)

Open AccessArticle Fructose Rich Diet-Induced High Plasminogen Activator Inhibitor-1 (PAI-1) Production in the Adult Female Rat: Protective Effect of Progesterone

by Daniel Castrogiovanni, Ana Alzamendi, Luisina Ongaro, Andrés Giovambattista, Rolf C. Gaillard and Eduardo Spinedi

Nutrients 2012, 4(8), 1137-1150; doi:10.3390/nu4081137

Received: 24 May 2012 / Revised: 20 July 2012 / Accepted: 8 August 2012 / Published: 22 August 2012

Cited by 4 | PDF Full-text (243 KB) | HTML Full-text | XML Full-text

Abstract

The effect of progesterone (P4) on fructose rich diet (FRD) intake-induced metabolic, endocrine and parametrial adipose tissue (PMAT) dysfunctions was studied in the adult female rat. Sixty day-old rats were i.m. treated with oil alone (control, CT) or containing P4 (12 mg/kg). Rats ate Purina chow-diet ad libitum throughout the entire experiment and, between 100 and 120 days of age drank ad libitum tap water alone (normal diet; CT-ND and P4-ND) or containing fructose (10% w/v; CT-FRD and P4-FRD). At age 120 days, animals were subjected to a glucose tolerance test or decapitated. Plasma concentrations of various biomarkers and PMAT gene abundance were monitored. P4-ND (vs. CT-ND) rats showed elevated circulating levels of lipids. CT-FRD rats displayed high (vs. CT-ND) plasma concentrations of lipids, leptin, adiponectin and plasminogen activator inhibitor-1 (PAI-1). Lipidemia and adiponectinemia were high (vs. P4-ND) in P4-FRD rats. Although P4 failed to prevent FRD-induced hyperleptinemia, it was fully protective on FRD-enhanced plasma PAI-1 levels. PMAT leptin and adiponectin mRNAs were high in CT-FRD and P4-FRD rats. While FRD enhanced PMAT PAI-1 mRNA abundance in CT rats, this effect was absent in P4 rats. Our study supports that a preceding P4-enriched milieu prevented the enhanced prothrombotic risk induced by FRD-elicited high PAI-1 production. Full article

(This article belongs to the Special Issue Nutrigenetics and Nutrigenomics)

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Review

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Open AccessReview Genomic and Epigenomic Insights into Nutrition and Brain Disorders

by Margaret Joy Dauncey

Nutrients 2013, 5(3), 887-914; doi:10.3390/nu5030887

Received: 25 January 2013 / Revised: 28 February 2013 / Accepted: 8 March 2013 / Published: 15 March 2013

Cited by 18 | PDF Full-text (547 KB) | HTML Full-text | XML Full-text

Abstract

Considerable evidence links many neuropsychiatric, neurodevelopmental and neurodegenerative disorders with multiple complex interactions between genetics and environmental factors such as nutrition. Mental health problems, autism, eating disorders, Alzheimer’s disease, schizophrenia, Parkinson’s disease and brain tumours are related to individual variability in numerous protein-coding and non-coding regions of the genome. However, genotype does not necessarily determine neurological phenotype because the epigenome modulates gene expression in response to endogenous and exogenous regulators, throughout the life-cycle. Studies using both genome-wide analysis of multiple genes and comprehensive analysis of specific genes are providing new insights into genetic and epigenetic mechanisms underlying nutrition and neuroscience. This review provides a critical evaluation of the following related areas: (1) recent advances in genomic and epigenomic technologies, and their relevance to brain disorders; (2) the emerging role of non-coding RNAs as key regulators of transcription, epigenetic processes and gene silencing; (3) novel approaches to nutrition, epigenetics and neuroscience; (4) gene-environment interactions, especially in the serotonergic system, as a paradigm of the multiple signalling pathways affected in neuropsychiatric and neurological disorders. Current and future advances in these four areas should contribute significantly to the prevention, amelioration and treatment of multiple devastating brain disorders. Full article

(This article belongs to the Special Issue Nutrigenetics and Nutrigenomics)

Open AccessReview Nutrigenetics and Metabolic Disease: Current Status and Implications for Personalised Nutrition

by Catherine M. Phillips

Nutrients 2013, 5(1), 32-57; doi:10.3390/nu5010032

Received: 30 September 2012 / Revised: 12 December 2012 / Accepted: 21 December 2012 / Published: 10 January 2013

Cited by 40 | PDF Full-text (476 KB) | HTML Full-text | XML Full-text

Abstract

Obesity, particularly central adiposity, is the primary causal factor in the development of insulin resistance, the hallmark of the metabolic syndrome (MetS), a common condition characterized by dyslipidaemia and hypertension, which is associated with increased risk of cardiovascular disease (CVD) and type 2 diabetes (T2DM). Interactions between genetic and environmental factors such as diet and lifestyle, particularly over-nutrition and sedentary behavior, promote the progression and pathogenesis of these polygenic diet-related diseases. Their current prevalence is increasing dramatically to epidemic proportions. Nutrition is probably the most important environmental factor that modulates expression of genes involved in metabolic pathways and the variety of phenotypes associated with obesity, the MetS and T2DM. Furthermore, the health effects of nutrients may be modulated by genetic variants. Nutrigenomics and nutrigenetics require an understanding of nutrition, genetics, biochemistry and a range of “omic” technologies to investigate the complex interaction between genetic and environmental factors relevant to metabolic health and disease. These rapidly developing fields of nutritional science hold much promise in improving nutrition for optimal personal and public health. This review presents the current state of the art in nutrigenetic research illustrating the significance of gene-nutrient interactions in the context of metabolic disease. Full article

(This article belongs to the Special Issue Nutrigenetics and Nutrigenomics)

Open AccessReview Molecular Nutrition Research—The Modern Way Of Performing Nutritional Science

by Frode Norheim, Ingrid M. F. Gjelstad, Marit Hjorth, Kathrine J. Vinknes, Torgrim M. Langleite, Torgeir Holen, Jørgen Jensen, Knut Tomas Dalen, Anette S. Karlsen, Anders Kielland, Arild C. Rustan and Christian A. Drevon

Nutrients 2012, 4(12), 1898-1944; doi:10.3390/nu4121898

Received: 6 September 2012 / Revised: 25 October 2012 / Accepted: 12 November 2012 / Published: 3 December 2012

Cited by 21 | PDF Full-text (1154 KB) | HTML Full-text | XML Full-text

Abstract

In spite of amazing progress in food supply and nutritional science, and a striking increase in life expectancy of approximately 2.5 months per year in many countries during the previous 150 years, modern nutritional research has a great potential of still contributing to improved health for future generations, granted that the revolutions in molecular and systems technologies are applied to nutritional questions. Descriptive and mechanistic studies using state of the art epidemiology, food intake registration, genomics with single nucleotide polymorphisms (SNPs) and epigenomics, transcriptomics, proteomics, metabolomics, advanced biostatistics, imaging, calorimetry, cell biology, challenge tests (meals, exercise, etc.), and integration of all data by systems biology, will provide insight on a much higher level than today in a field we may name molecular nutrition research. To take advantage of all the new technologies scientists should develop international collaboration and gather data in large open access databases like the suggested Nutritional Phenotype database (dbNP). This collaboration will promote standardization of procedures (SOP), and provide a possibility to use collected data in future research projects. The ultimate goals of future nutritional research are to understand the detailed mechanisms of action for how nutrients/foods interact with the body and thereby enhance health and treat diet-related diseases. Full article

(This article belongs to the Special Issue Nutrigenetics and Nutrigenomics)

Open AccessReview Dietary Regulation of Histone Acetylases and Deacetylases for the Prevention of Metabolic Diseases

by Tho X. Pham and Jiyoung Lee

Nutrients 2012, 4(12), 1868-1886; doi:10.3390/nu4121868

Received: 1 October 2012 / Revised: 12 November 2012 / Accepted: 22 November 2012 / Published: 28 November 2012

Cited by 23 | PDF Full-text (429 KB) | HTML Full-text | XML Full-text

Abstract

Age-related diseases such as type 2 diabetes, cardiovascular disease, and cancer involve epigenetic modifications, where accumulation of minute changes in the epigenome over time leads to disease manifestation. Epigenetic changes are influenced by life style and diets. This represents an avenue whereby dietary components could accelerate or prevent age-related diseases through their effects on epigenetic modifications. Histone acetylation is an epigenetic modification that is regulated through the opposing action of histone acetylases (HATs) and deacetylases (HDACs). These two families of enzymes play critical roles in metabolic processes and their dysregulation is associated with pathogenesis of several diseases. Dietary components, such as butyrate, sulforaphane, and curcumin, have been shown to affect HAT and HDAC activity, and their health benefits are attributed, at least in part, to epigenetic modifications. Given the decades that it takes to accumulate epigenetic changes, it is unlikely that pharmaceuticals could undo epigenetic changes without side effects. Therefore, long term consumption of dietary components that can alter the epigenome could be an attractive means of disease prevention. The goal of this review is to highlight the roles of diets and food components in epigenetic modifications through the regulation of HATs and HDACs for disease prevention. Full article

(This article belongs to the Special Issue Nutrigenetics and Nutrigenomics)

Open AccessReview Lipophilic Micronutrients and Adipose Tissue Biology

by Jean-François Landrier, Julie Marcotorchino and Franck Tourniaire

Nutrients 2012, 4(11), 1622-1649; doi:10.3390/nu4111622

Received: 5 September 2012 / Revised: 6 October 2012 / Accepted: 27 October 2012 / Published: 6 November 2012

Cited by 22 | PDF Full-text (578 KB) | HTML Full-text | XML Full-text

Abstract

Lipophilic micronutrients (LM) constitute a large family of molecules including several vitamins (A, D, E, K) and carotenoids. Their ability to regulate gene expression is becoming increasingly clear and constitutes an important part of nutrigenomics. Interestingly, adipose tissue is not only a main storage site for these molecules within the body, but it is also subjected to the regulatory effects of LM. Indeed, several gene regulations have been described in adipose tissue that could strongly impact its biology with respect to the modulation of adipogenesis, inflammatory status, or energy homeostasis and metabolism, among others. The repercussions in terms of health effects of such regulations in the context of obesity and associated pathologies represent an exciting and emerging field of research. The present review will focus on the regulatory effects of vitamin A, D, E and K as well as carotenoids on adipose tissue biology and physiology, notably in the context of obesity and associated disorders. Full article

(This article belongs to the Special Issue Nutrigenetics and Nutrigenomics)

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