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Nutritional Epigenetics

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

Deadline for manuscript submissions: closed (30 June 2014) | Viewed by 184739

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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
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Guest Editor
Liggins Institute, University of Auckland, Auckland 1023, New Zealand
Interests: spatial genome organization; the epigenome; gene looping; microbiome; fetal epigenetics, maternal influence

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Keywords

  • diet
  • epigenetics
  • fetal programming

Published Papers (13 papers)

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Research

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198 KiB  
Article
Nutrients Intake Is Associated with DNA Methylation of Candidate Inflammatory Genes in a Population of Obese Subjects
by Valentina Bollati, Chiara Favero, Benedetta Albetti, Letizia Tarantini, Alice Moroni, Hyang-Min Byun, Valeria Motta, Diana Misaela Conti, Amedea Silvia Tirelli, Luisella Vigna, Pier Alberto Bertazzi and Angela Cecilia Pesatori
Nutrients 2014, 6(10), 4625-4639; https://doi.org/10.3390/nu6104625 - 22 Oct 2014
Cited by 42 | Viewed by 7999
Abstract
The aim of the present study was to evaluate the potential association between dietary nutrients and alterations in DNA methylation in a set of five candidate genes, including CD14, Et-1, iNOS, HERV-w and TNFα, in a population of overweight/obese subjects. We evaluated possible [...] Read more.
The aim of the present study was to evaluate the potential association between dietary nutrients and alterations in DNA methylation in a set of five candidate genes, including CD14, Et-1, iNOS, HERV-w and TNFα, in a population of overweight/obese subjects. We evaluated possible associations between gene methylation and clinical blood parameters, including total cholesterol (TC), low- and high-density lipoprotein cholesterol (LDL-C and HDL-C), triglyceride and homocysteine levels. We employed validated methods to assess anthropometric, clinical and dietary data, as well as pyrosequencing to evaluate DNA methylation of the five candidate genes in 165 overweight/obese subjects. There was no association between body mass index and DNA methylation of the five candidate genes in this group of subjects. Positive associations were observed between TNFα methylation and blood levels of LDL-C (β = 0.447, p = 0.002), TC/HDL-C (β = 0.467, p = 0.001) and LDL-C/HDL-C (β = 0.445, p = 0.002), as well as between HERV-w methylation and dietary intakes of β-carotene (β = 0.088, p = 0.051) and carotenoids (β = 0.083, p = 0.029). TNFα methylation showed negative associations with dietary intakes of cholesterol (β = −0.278, p = 0.048), folic acid (β = −0.339, p = 0.012), β-carotene (β = −0.332, p = 0.045), carotenoids (β = −0.331, p = 0.015) and retinol (β = −0.360, p = 0.008). These results suggest a complex relationship among nutrient intake, oxidative stress and DNA methylation. Full article
(This article belongs to the Special Issue Nutritional Epigenetics)
216 KiB  
Article
Protein Content and Methyl Donors in Maternal Diet Interact to Influence the Proliferation Rate and Cell Fate of Neural Stem Cells in Rat Hippocampus
by Valérie Amarger, Angèle Lecouillard, Laure Ancellet, Isabelle Grit, Blandine Castellano, Philippe Hulin and Patricia Parnet
Nutrients 2014, 6(10), 4200-4217; https://doi.org/10.3390/nu6104200 - 14 Oct 2014
Cited by 14 | Viewed by 8925
Abstract
Maternal diet during pregnancy and early postnatal life influences the setting up of normal physiological functions in the offspring. Epigenetic mechanisms regulate cell differentiation during embryonic development and may mediate gene/environment interactions. We showed here that high methyl donors associated with normal protein [...] Read more.
Maternal diet during pregnancy and early postnatal life influences the setting up of normal physiological functions in the offspring. Epigenetic mechanisms regulate cell differentiation during embryonic development and may mediate gene/environment interactions. We showed here that high methyl donors associated with normal protein content in maternal diet increased the in vitro proliferation rate of neural stem/progenitor cells isolated from rat E19 fetuses. Gene expression on whole hippocampi at weaning confirmed this effect as evidenced by the higher expression of the Nestin and Igf2 genes, suggesting a higher amount of undifferentiated precursor cells. Additionally, protein restriction reduced the expression of the insulin receptor gene, which is essential to the action of IGFII. Inhibition of DNA methylation in neural stem/progenitor cells in vitro increased the expression of the astrocyte-specific Gfap gene and decreased the expression of the neuron-specific Dcx gene, suggesting an impact on cell differentiation. Our data suggest a complex interaction between methyl donors and protein content in maternal diet that influence the expression of major growth factors and their receptors and therefore impact the proliferation and differentiation capacities of neural stem cells, either through external hormone signals or internal genomic regulation. Full article
(This article belongs to the Special Issue Nutritional Epigenetics)
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422 KiB  
Article
DNA Hypermethylation of the Serotonin Receptor Type-2A Gene Is Associated with a Worse Response to a Weight Loss Intervention in Subjects with Metabolic Syndrome
by Aurora Perez-Cornago, Maria L. Mansego, María Angeles Zulet and José Alfredo Martinez
Nutrients 2014, 6(6), 2387-2403; https://doi.org/10.3390/nu6062387 - 23 Jun 2014
Cited by 21 | Viewed by 7794
Abstract
Understanding the regulation of gene activities depending on DNA methylation has been the subject of much recent study. However, although polymorphisms of the HTR2A gene have been associated with both obesity and psychiatric disorders, the role of HTR2A gene methylation in these illnesses [...] Read more.
Understanding the regulation of gene activities depending on DNA methylation has been the subject of much recent study. However, although polymorphisms of the HTR2A gene have been associated with both obesity and psychiatric disorders, the role of HTR2A gene methylation in these illnesses remains uncertain. The aim of this study was to evaluate the association of HTR2A gene promoter methylation levels in white blood cells (WBC) with obesity traits and depressive symptoms in individuals with metabolic syndrome (MetS) enrolled in a behavioural weight loss programme. Analyses were based on 41 volunteers (mean age 49 ± 1 year) recruited within the RESMENA study. Depressive symptoms (as determined using the Beck Depression Inventory), anthropometric and biochemical measurements were analysed at the beginning and after six months of weight loss treatment. At baseline, DNA from WBC was isolated and cytosine methylation in the HTR2A gene promoter was quantified by a microarray approach. In the whole-study sample, a positive association of HTR2A gene methylation with waist circumference and insulin levels was detected at baseline. Obesity measures significantly improved after six months of dietary treatment, where a lower mean HTR2A gene methylation at baseline was associated with major reductions in body weight, BMI and fat mass after the treatment. Moreover, mean HTR2A gene methylation at baseline significantly predicted the decrease in depressive symptoms after the weight loss treatment. In conclusion, this study provides newer evidence that hypermethylation of the HTR2A gene in WBC at baseline is significantly associated with a worse response to a weight-loss intervention and with a lower decrease in depressive symptoms after the dietary treatment in subjects with MetS. Full article
(This article belongs to the Special Issue Nutritional Epigenetics)
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Review

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144 KiB  
Review
What Do Studies of Insect Polyphenisms Tell Us about Nutritionally-Triggered Epigenomic Changes and Their Consequences?
by Andrew G. Cridge, Megan P. Leask, Elizabeth J. Duncan and Peter K. Dearden
Nutrients 2015, 7(3), 1787-1797; https://doi.org/10.3390/nu7031787 - 11 Mar 2015
Cited by 19 | Viewed by 11862
Abstract
Many insects are capable of remarkable changes in biology and form in response to their environment or diet. The most extreme example of these are polyphenisms, which are when two or more different phenotypes are produced from a single genotype in response to [...] Read more.
Many insects are capable of remarkable changes in biology and form in response to their environment or diet. The most extreme example of these are polyphenisms, which are when two or more different phenotypes are produced from a single genotype in response to the environment. Polyphenisms provide a fascinating opportunity to study how the environment affects an animal’s genome, and how this produces changes in form. Here we review the current state of knowledge of the molecular basis of polyphenisms and what can be learnt from them to understand how nutrition may influence our own genomes. Full article
(This article belongs to the Special Issue Nutritional Epigenetics)
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305 KiB  
Review
The Interaction between Epigenetics, Nutrition and the Development of Cancer
by Karen S. Bishop and Lynnette R. Ferguson
Nutrients 2015, 7(2), 922-947; https://doi.org/10.3390/nu7020922 - 30 Jan 2015
Cited by 140 | Viewed by 25062
Abstract
Unlike the genome, the epigenome can be modified and hence some epigenetic risk markers have the potential to be reversed. Such modifications take place by means of drugs, diet or environmental exposures. It is widely accepted that epigenetic modifications take place during early [...] Read more.
Unlike the genome, the epigenome can be modified and hence some epigenetic risk markers have the potential to be reversed. Such modifications take place by means of drugs, diet or environmental exposures. It is widely accepted that epigenetic modifications take place during early embryonic and primordial cell development, but it is also important that we gain an understanding of the potential for such changes later in life. These “later life” epigenetic modifications in response to dietary intervention are the focus of this paper. The epigenetic modifications investigated include DNA methylation, histone modifications and the influence of microRNAs. The epigenotype could be used not only to predict susceptibility to certain cancers but also to assess the effectiveness of dietary modifications to reduce such risk. The influence of diet or dietary components on epigenetic modifications and the impact on cancer initiation or progression has been assessed herein. Full article
(This article belongs to the Special Issue Nutritional Epigenetics)
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179 KiB  
Review
Insights from Space: Potential Role of Diet in the Spatial Organization of Chromosomes
by Justin M. O'Sullivan, Malina D. Doynova, Jisha Antony, Florian Pichlmuller and Julia A. Horsfield
Nutrients 2014, 6(12), 5724-5739; https://doi.org/10.3390/nu6125724 - 10 Dec 2014
Cited by 3 | Viewed by 6737
Abstract
We can now sequence and identify genome wide epigenetic patterns and perform a variety of “genomic experiments” within relatively short periods of time—ranging from days to weeks. Yet, despite these technological advances, we have a poor understanding of the inter-relationships between epigenetics, genome [...] Read more.
We can now sequence and identify genome wide epigenetic patterns and perform a variety of “genomic experiments” within relatively short periods of time—ranging from days to weeks. Yet, despite these technological advances, we have a poor understanding of the inter-relationships between epigenetics, genome structure-function, and nutrition. Perhaps this limitation lies, in part, in our propensity to study epigenetics in terms of the linear arrangement of elements and genes. Here we propose that a more complete understanding of how nutrition impacts on epigenetics and cellular development resides within the inter-relationships between DNA and histone modification patterns and genome function, in the context of spatial organization of chromatin and the epigenome. Full article
(This article belongs to the Special Issue Nutritional Epigenetics)
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423 KiB  
Review
The Role of Dietary Histone Deacetylases (HDACs) Inhibitors in Health and Disease
by Shalome A. Bassett and Matthew P. G. Barnett
Nutrients 2014, 6(10), 4273-4301; https://doi.org/10.3390/nu6104273 - 15 Oct 2014
Cited by 136 | Viewed by 17468
Abstract
Modification of the histone proteins associated with DNA is an important process in the epigenetic regulation of DNA structure and function. There are several known modifications to histones, including methylation, acetylation, and phosphorylation, and a range of factors influence each of these. Histone [...] Read more.
Modification of the histone proteins associated with DNA is an important process in the epigenetic regulation of DNA structure and function. There are several known modifications to histones, including methylation, acetylation, and phosphorylation, and a range of factors influence each of these. Histone deacetylases (HDACs) remove the acetyl group from lysine residues within a range of proteins, including transcription factors and histones. Whilst this means that their influence on cellular processes is more complex and far-reaching than histone modifications alone, their predominant function appears to relate to histones; through deacetylation of lysine residues they can influence expression of genes encoded by DNA linked to the histone molecule. HDAC inhibitors in turn regulate the activity of HDACs, and have been widely used as therapeutics in psychiatry and neurology, in which a number of adverse outcomes are associated with aberrant HDAC function. More recently, dietary HDAC inhibitors have been shown to have a regulatory effect similar to that of pharmacological HDAC inhibitors without the possible side-effects. Here, we discuss a number of dietary HDAC inhibitors, and how they may have therapeutic potential in the context of a whole food. Full article
(This article belongs to the Special Issue Nutritional Epigenetics)
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998 KiB  
Review
Impact of Soy Isoflavones on the Epigenome in Cancer Prevention
by Maria Pudenz, Kevin Roth and Clarissa Gerhauser
Nutrients 2014, 6(10), 4218-4272; https://doi.org/10.3390/nu6104218 - 15 Oct 2014
Cited by 77 | Viewed by 15946
Abstract
Isoflavones (IF) such as genistein are cancer preventive phytochemicals found in soy and other legumes. Epidemiological studies point to a reduced risk for hormone‑dependent cancers in populations following a typical Asian diet rich in soy products. IF act as phytoestrogens and prevent tumorigenesis [...] Read more.
Isoflavones (IF) such as genistein are cancer preventive phytochemicals found in soy and other legumes. Epidemiological studies point to a reduced risk for hormone‑dependent cancers in populations following a typical Asian diet rich in soy products. IF act as phytoestrogens and prevent tumorigenesis in rodent models by a broad spectrum of bioactivities. During the past 10 years, IF were shown to target all major epigenetic mechanisms regulating gene expression, including DNA methylation, histone modifications controlling chromatin accessibility, and non-coding RNAs. These effects have been suggested to contribute to cancer preventive potential in in vitro and in vivo studies, affecting several key processes such as DNA repair, cell signaling cascades including Wnt-signaling, induction of apoptosis, cell cycle progression, cell proliferation, migration and invasion, epithelial-mesenchymal transition (EMT), metastasis formation and development of drug-resistance. We here summarize the state-of-the-art of IF affecting the epigenome in major hormone-dependent, urogenital, and gastrointestinal tumor types and in in vivo studies on anti-cancer treatment or developmental aspects, and short-term intervention studies in adults. These data, while often requiring replication, suggest that epigenetic gene regulation represents an important novel target of IF and should be taken into consideration when evaluating the cancer preventive potential of IF in humans. Full article
(This article belongs to the Special Issue Nutritional Epigenetics)
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314 KiB  
Review
Epigenetic Mechanisms Underlying the Link between Non-Alcoholic Fatty Liver Diseases and Nutrition
by Joo Ho Lee, Simonetta Friso and Sang-Woon Choi
Nutrients 2014, 6(8), 3303-3325; https://doi.org/10.3390/nu6083303 - 21 Aug 2014
Cited by 98 | Viewed by 13415
Abstract
Non-alcoholic fatty liver disease (NAFLD) is defined as a pathologic accumulation of fat in the form of triglycerides (TG) in the liver (steatosis) that is not caused by alcohol. A subgroup of NAFLD patients shows liver cell injury and inflammation coupled with the [...] Read more.
Non-alcoholic fatty liver disease (NAFLD) is defined as a pathologic accumulation of fat in the form of triglycerides (TG) in the liver (steatosis) that is not caused by alcohol. A subgroup of NAFLD patients shows liver cell injury and inflammation coupled with the excessive fat accumulation (steatohepatitis), which is referred to as non-alcoholic steatohepatitis (NASH). Patients with NASH may develop cirrhosis and hepatocellular carcinoma (HCC). NAFLD shares the key features of metabolic syndrome including obesity, hyperlipidemia, hypertension, and insulin resistance. The pathogenesis of NAFLD is multi-factorial, however the oxidative stress seems to plays a major role in the development and progression of the disease. The emerging field of epigenetics provides a new perspective on the pathogenesis of NAFLD. Epigenetics is an inheritable but reversible phenomenon that affects gene expression without altering the DNA sequence and refers to DNA methylation, histone modifications and microRNAs. Epigenetic manipulation through metabolic pathways such as one-carbon metabolism has been proposed as a promising approach to retard the progression of NAFLD. Investigating the epigenetic modifiers in NAFLD may also lead to the development of preventive or therapeutic strategies for NASH-associated complications. Full article
(This article belongs to the Special Issue Nutritional Epigenetics)
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203 KiB  
Review
Early Life Nutrition, Epigenetics and Programming of Later Life Disease
by Mark H. Vickers
Nutrients 2014, 6(6), 2165-2178; https://doi.org/10.3390/nu6062165 - 2 Jun 2014
Cited by 268 | Viewed by 24412
Abstract
The global pandemic of obesity and type 2 diabetes is often causally linked to marked changes in diet and lifestyle; namely marked increases in dietary intakes of high energy diets and concomitant reductions in physical activity levels. However, less attention has been paid [...] Read more.
The global pandemic of obesity and type 2 diabetes is often causally linked to marked changes in diet and lifestyle; namely marked increases in dietary intakes of high energy diets and concomitant reductions in physical activity levels. However, less attention has been paid to the role of developmental plasticity and alterations in phenotypic outcomes resulting from altered environmental conditions during the early life period. Human and experimental animal studies have highlighted the link between alterations in the early life environment and increased risk of obesity and metabolic disorders in later life. This link is conceptualised as the developmental programming hypothesis whereby environmental influences during critical periods of developmental plasticity can elicit lifelong effects on the health and well-being of the offspring. In particular, the nutritional environment in which the fetus or infant develops influences the risk of metabolic disorders in offspring. The late onset of such diseases in response to earlier transient experiences has led to the suggestion that developmental programming may have an epigenetic component, as epigenetic marks such as DNA methylation or histone tail modifications could provide a persistent memory of earlier nutritional states. Moreover, evidence exists, at least from animal models, that such epigenetic programming should be viewed as a transgenerational phenomenon. However, the mechanisms by which early environmental insults can have long-term effects on offspring are relatively unclear. Thus far, these mechanisms include permanent structural changes to the organ caused by suboptimal levels of an important factor during a critical developmental period, changes in gene expression caused by epigenetic modifications (including DNA methylation, histone modification, and microRNA) and permanent changes in cellular ageing. A better understanding of the epigenetic basis of developmental programming and how these effects may be transmitted across generations is essential for the implementation of initiatives aimed at curbing the current obesity and diabetes crisis. Full article
(This article belongs to the Special Issue Nutritional Epigenetics)
215 KiB  
Review
Epigenetic Effects of Human Breast Milk
by Elvira Verduci, Giuseppe Banderali, Salvatore Barberi, Giovanni Radaelli, Alessandra Lops, Federica Betti, Enrica Riva and Marcello Giovannini
Nutrients 2014, 6(4), 1711-1724; https://doi.org/10.3390/nu6041711 - 24 Apr 2014
Cited by 138 | Viewed by 20395
Abstract
A current aim of nutrigenetics is to personalize nutritional practices according to genetic variations that influence the way of digestion and metabolism of nutrients introduced with the diet. Nutritional epigenetics concerns knowledge about the effects of nutrients on gene expression. Nutrition in early [...] Read more.
A current aim of nutrigenetics is to personalize nutritional practices according to genetic variations that influence the way of digestion and metabolism of nutrients introduced with the diet. Nutritional epigenetics concerns knowledge about the effects of nutrients on gene expression. Nutrition in early life or in critical periods of development, may have a role in modulating gene expression, and, therefore, have later effects on health. Human breast milk is well-known for its ability in preventing several acute and chronic diseases. Indeed, breastfed children may have lower risk of neonatal necrotizing enterocolitis, infectious diseases, and also of non-communicable diseases, such as obesity and related-disorders. Beneficial effects of human breast milk on health may be associated in part with its peculiar components, possible also via epigenetic processes. This paper discusses about presumed epigenetic effects of human breast milk and components. While evidence suggests that a direct relationship may exist of some components of human breast milk with epigenetic changes, the mechanisms involved are still unclear. Studies have to be conducted to clarify the actual role of human breast milk on genetic expression, in particular when linked to the risk of non-communicable diseases, to potentially benefit the infant’s health and his later life. Full article
(This article belongs to the Special Issue Nutritional Epigenetics)

Other

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1571 KiB  
Case Report
Resveratrol Based Oral Nutritional Supplement Produces Long-Term Beneficial Effects on Structure and Visual Function in Human Patients
by Stuart Richer, Shana Patel, Shivani Sockanathan, Lawrence J. Ulanski II, Luke Miller and Carla Podella
Nutrients 2014, 6(10), 4404-4420; https://doi.org/10.3390/nu6104404 - 17 Oct 2014
Cited by 52 | Viewed by 10552
Abstract
Background: Longevinex® (L/RV) is a low dose hormetic over-the-counter (OTC) oral resveratrol (RV) based matrix of red wine solids, vitamin D3 and inositol hexaphosphate (IP6) with established bioavailability, safety, and short-term efficacy against the earliest signs of human atherosclerosis, murine cardiac [...] Read more.
Background: Longevinex® (L/RV) is a low dose hormetic over-the-counter (OTC) oral resveratrol (RV) based matrix of red wine solids, vitamin D3 and inositol hexaphosphate (IP6) with established bioavailability, safety, and short-term efficacy against the earliest signs of human atherosclerosis, murine cardiac reperfusion injury, clinical retinal neovascularization, and stem cell survival. We previously reported our short-term findings for dry and wet age-related macular degeneration (AMD) patients. Today we report long term (two to three year) clinical efficacy. Methods: We treated three patients including a patient with an AMD treatment resistant variant (polypoidal retinal vasculature disease). We evaluated two clinical measures of ocular structure (fundus autofluorescent imaging and spectral domain optical coherence extended depth choroidal imaging) and qualitatively appraised changes in macular pigment volume. We further evaluated three clinical measures of visual function (Snellen visual acuity, contrast sensitivity, and glare recovery to a cone photo-stress stimulus). Results: We observed broad bilateral improvements in ocular structure and function over a long time period, opposite to what might be expected due to aging and the natural progression of the patient’s pathophysiology. No side effects were observed. Conclusions: These three cases demonstrate that application of epigenetics has long-term efficacy against AMD retinal disease, when the retinal specialist has exhausted other therapeutic modalities. Full article
(This article belongs to the Special Issue Nutritional Epigenetics)
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501 KiB  
Concept Paper
Selenium-Enriched Foods Are More Effective at Increasing Glutathione Peroxidase (GPx) Activity Compared with Selenomethionine: A Meta-Analysis
by Emma N. Bermingham, John E. Hesketh, Bruce R. Sinclair, John P. Koolaard and Nicole C. Roy
Nutrients 2014, 6(10), 4002-4031; https://doi.org/10.3390/nu6104002 - 29 Sep 2014
Cited by 61 | Viewed by 12208
Abstract
Selenium may play a beneficial role in multi-factorial illnesses with genetic and environmental linkages via epigenetic regulation in part via glutathione peroxidase (GPx) activity. A meta-analysis was undertaken to quantify the effects of dietary selenium supplementation on the activity of overall GPx activity [...] Read more.
Selenium may play a beneficial role in multi-factorial illnesses with genetic and environmental linkages via epigenetic regulation in part via glutathione peroxidase (GPx) activity. A meta-analysis was undertaken to quantify the effects of dietary selenium supplementation on the activity of overall GPx activity in different tissues and animal species and to compare the effectiveness of different forms of dietary selenium. GPx activity response was affected by both the dose and form of selenium (p < 0.001). There were differences between tissues on the effects of selenium supplementation on GPx activity (p < 0.001); however, there was no evidence in the data of differences between animal species (p = 0.95). The interactions between dose and tissue, animal species and form were significant (p < 0.001). Tissues particularly sensitive to changes in selenium supply include red blood cells, kidney and muscle. The meta-analysis identified that for animal species selenium-enriched foods were more effective than selenomethionine at increasing GPx activity. Full article
(This article belongs to the Special Issue Nutritional Epigenetics)
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