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Nutrients
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Dietary Intake and Gluten-Associated Disease
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Dietary Intake and Gluten-Associated Disease

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

Deadline for manuscript submissions: closed (31 August 2019) | Viewed by 41947

Special Issue Editor

Prof. Dr. Yurdagül Zopf

E-Mail Website
Guest Editor
1. Department of Medicine 1, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg, 91054 Erlangen, Germany
2. Hector-Center for Nutrition, Exercise and Sports, Department of Medicine 1, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg, 91054 Erlangen, Germany
3. German Center Immunotherapy (DZI), University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg, 91054 Erlangen, Germany
Interests: cachexia syndrome; malnutrition; muscle function; atrophy and therapy; food intolerance and food allergy; celiac disease and non-celiac gluten sensitivity; chronic inflammatory bowel disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In recent years, the influence of diet on the occurrence and treatment of many diseases has become more and more apparent. In particular, the effect of gluten on health has been increasingly studied, bith clinically and scientifically. The following Special Issue discusses the effect of gluten and gluten-associated proteins, such as amylase trypsin inhibitors (ATI), as well as food groups such as FODMAPs on the intestinal mucosa. The association of gluten consumption and irritable bowel syndrome (IBS) will be elucidated and the influence of fructans will be discussed. Recent data in gluten-sensitive patients have shown that a gluten-free diet positively influences the inflammation in the small intestine.

The FODMAP-reduced diet appears to be less effective in treating the symptoms in gluten-sensitivity compared to irritable bowel syndrome. The elimination of gluten from the diet seems to be rather easy to manage in the Western world because of the availability of gluten-free pseudocereals such as millet, amaranth, quinoa, and buckwheat, in addition to many commercially available gluten-free products. However, an increased risk of malnutrition or malnutrition and complications resulting from a gluten-free diet is frequently discussed. The articles in this edition will present a detailed overview of the scientific knowledge regarding the difficulties and consequences of a gluten-free diet.

Since the prevalence of gluten intolerance has increased over the last few decades, it has been hypothesized that, over the years, the adaptation of the relevant cereals to the environment is the main cause of patient discomfort.

In this Special Issue, the current results of gluten content in numerous cereals from different decades will be presented and their influence on nutritional therapy will be discussed.

Prof. Yurdagül Zopf
Guest Editor

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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

Gluten

Celiac disease

IBS

ATI

Diet

Inflammation

Nutrition

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Published Papers (5 papers)

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Research

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21 pages, 6240 KiB  
Article
Gliadin Intake Causes Disruption of the Intestinal Barrier and an Increase in Germ Cell Apoptosis in A Caenorhabditis Elegans Model
by Hyemin Min, Ji-Sun Kim, Jiyun Ahn and Yhong-Hee Shim
Nutrients 2019, 11(11), 2587; https://doi.org/10.3390/nu11112587 - 27 Oct 2019
Cited by 10 | Viewed by 4955
Abstract
Gliadin is a major protein component of gluten and causes gluten toxicity through intestinal stress. We previously showed that gliadin intake induces oxidative stress in the intestine and reduces fertility in a Caenorhabditis elegans model. To elucidate the possible link between intestinal stress [...] Read more.
Gliadin is a major protein component of gluten and causes gluten toxicity through intestinal stress. We previously showed that gliadin intake induces oxidative stress in the intestine and reduces fertility in a Caenorhabditis elegans model. To elucidate the possible link between intestinal stress and reproduction, changes in the intestine and germ cells of C. elegans after gliadin intake were examined at the molecular level. Gliadin intake increased reactive oxygen species (ROS) production in the intestine, decreased intestinal F-actin levels, and increased germ cell apoptosis. These gliadin-triggered effects were suppressed by antioxidant treatment. These results suggest that ROS production in the intestine induced by gliadin intake causes disruption of intestinal integrity and increases germ cell apoptosis. Gliadin-induced germ cell apoptosis (GIGA) was suppressed by depletion of cep-1, ced-13, egl-1, or mpk-1. However, HUS-1 was not activated, suggesting that GIGA is activated through the mitogen-activated protein kinase (MAPK) pathway and is CEP-1-dependent but is a separate pathway from that controlling the DNA damage response. Taken together, our results suggest that gliadin causes intestinal barrier disruption through ROS production and interacts with the germ cells to reduce fertility through GIGA. Full article
(This article belongs to the Special Issue Dietary Intake and Gluten-Associated Disease)
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25 pages, 2563 KiB  
Article
Comprehensive Detection of Isopeptides between Human Tissue Transglutaminase and Gluten Peptides
by Barbara Lexhaller, Christina Ludwig and Katharina A. Scherf
Nutrients 2019, 11(10), 2263; https://doi.org/10.3390/nu11102263 - 20 Sep 2019
Cited by 15 | Viewed by 6019
Abstract
Celiac disease (CD) is a chronic inflammation of the small intestine triggered by the ingestion of gluten in genetically predisposed individuals. Tissue transglutaminase (TG2) is a key factor in CD pathogenesis, because it catalyzes both the deamidation of specific glutamine residues and the [...] Read more.
Celiac disease (CD) is a chronic inflammation of the small intestine triggered by the ingestion of gluten in genetically predisposed individuals. Tissue transglutaminase (TG2) is a key factor in CD pathogenesis, because it catalyzes both the deamidation of specific glutamine residues and the formation of covalent Nε-(γ-glutamyl)-lysine isopeptide crosslinks resulting in TG2–gluten peptide complexes. These complexes are thought to activate B cells causing the secretion of anti-TG2 autoantibodies that serve as diagnostic markers for CD, although their pathogenic role remains unclear. To gain more insight into the molecular structures of TG2-gluten peptide complexes, we used different proteomics software tools that enable the comprehensive identification of isopeptides. Thus, 34 different isopeptides involving 20 TG2 lysine residues were identified in a model system, only six of which were previously known. Additionally, 36 isopeptides of TG2-TG2 multimers were detected. Experiments with different TG2-gluten peptide molar ratios revealed the most preferred lysine residues involved in isopeptide crosslinking. Expanding the model system to three gluten peptides with more glutamine residues allowed the localization of the preferred glutamine crosslinking sites. These new insights into the structure of TG2-gluten peptide complexes may help clarify the role of extracellular TG2 in CD autoimmunity and in other inflammatory diseases. Full article
(This article belongs to the Special Issue Dietary Intake and Gluten-Associated Disease)
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12 pages, 445 KiB  
Communication
Gluten and FODMAPS—Sense of a Restriction/When Is Restriction Necessary?
by Walburga Dieterich and Yurdagül Zopf
Nutrients 2019, 11(8), 1957; https://doi.org/10.3390/nu11081957 - 20 Aug 2019
Cited by 30 | Viewed by 10962
Abstract
Gluten-free diet (GFD) is enjoying increasingly popularity, although gluten-free products are considerably more expensive. GFD is absolutely necessary for patients with celiac disease, as in this case even minor amounts of gluten can lead to the destruction of the intestinal mucosa. In addition, [...] Read more.
Gluten-free diet (GFD) is enjoying increasingly popularity, although gluten-free products are considerably more expensive. GFD is absolutely necessary for patients with celiac disease, as in this case even minor amounts of gluten can lead to the destruction of the intestinal mucosa. In addition, GFD is currently the best therapy to improve clinical symptoms of patients with non-celiac gluten sensitivity (NCGS), although the diet may not be as strict as that for patients with celiac disease. Beside gluten, other wheat components such as oligosaccharides and amylase trypsin inhibitors are discussed as triggers of NCGS in this review. An overlap between gastrointestinal symptoms in NCGS and irritable bowel syndrome (IBS) is described. Patients with NCGS attribute their symptoms to the consumption of gluten, while patients with IBS rarely describe gluten as a trigger. Recently, several studies have demonstrated that the introduction of a low FODMAP (fermentable oligo-, di-, monosaccharides, and polyols) diet reduced gastrointestinal symptoms in patients with IBS and this diet is suggested as the first choice of therapy in IBS. However, a low FODMAP diet also eliminates prebiotica and may negatively influence the gut microbiota. For this reason, the diet should be liberalized after symptom improvement. There is no evidence that a GFD is healthier than the standard diet. In contrast, GFD often is accompanied by nutritional deficiencies, mainly minerals and vitamins. Therefore, GFD and low FODMAP diets are not recommended for healthy subjects. Since wheat contains fructans belonging to FODMAPs), a GFD is not only gluten-free but also has less FODMAPs. Thus, symptom improvement cannot be correctly correlated with the reduction of either one or the other. Full article
(This article belongs to the Special Issue Dietary Intake and Gluten-Associated Disease)
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8 pages, 458 KiB  
Article
A Population Survey of Dietary Attitudes towards Gluten
by Iain D Croall, Nick Trott, Anupam Rej, Imran Aziz, David J O’Brien, Harvey A George, Mohammed Y Hossain, Lauren J S Marks, Jessica I Richardson, Rebecca Rigby, Marios Hadjivassiliou, Nigel Hoggard and David S Sanders
Nutrients 2019, 11(6), 1276; https://doi.org/10.3390/nu11061276 - 5 Jun 2019
Cited by 27 | Viewed by 8475
Abstract
It is unclear how the prevalence of people who believe the gluten-free diet (GFD) to be generally healthy (“Lifestylers”) is impacting the overall rates of self-reported gluten sensitivity (GS). We repeated a population survey from 2012 in order to examine how attitudes towards [...] Read more.
It is unclear how the prevalence of people who believe the gluten-free diet (GFD) to be generally healthy (“Lifestylers”) is impacting the overall rates of self-reported gluten sensitivity (GS). We repeated a population survey from 2012 in order to examine how attitudes towards GS have changed over time. Our survey (N = 1004) was administered in Sheffield (UK) in 2015, replicating the 2012 experiment. The questionnaire included a food frequency survey and assessed self-reported GS as well as associated variables (prevalence, current diet, pre-existing conditions, etc.). The overall rates of key variables and chi-squared analysis in comparison to the previous survey were as follows: self-reported GS was 32.8% (previously 12.9%, p < 0.001), pre-existing coeliac disease (CD) was 1.2% (previously 0.8%, p = 0.370), following a GFD was 3.7% (previously 3.7%, p = 0.997). Self-reported GS was positively associated with some pre-existing conditions, including anxiety, depression, chronic fatigue, headaches, and other food allergies/intolerances (including irritable bowel syndrome (IBS); chi-squared analyses, all p < 0.001). Over a 3-year period, the fraction of people who self-reported GS increased by over 250%. Despite this, arguably more meaningful indications of underlying physiological GS remained comparable. This research suggests that the public perception of gluten is causing a marked increase in the number of people who erroneously believe they are sensitive to it. Full article
(This article belongs to the Special Issue Dietary Intake and Gluten-Associated Disease)
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Review

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19 pages, 720 KiB  
Review
Intestinal Barrier Function in Gluten-Related Disorders
by Danielle Cardoso-Silva, Deborah Delbue, Alice Itzlinger, Renée Moerkens, Sebo Withoff, Federica Branchi and Michael Schumann
Nutrients 2019, 11(10), 2325; https://doi.org/10.3390/nu11102325 - 1 Oct 2019
Cited by 80 | Viewed by 10927
Abstract
Gluten-related disorders include distinct disease entities, namely celiac disease, wheat-associated allergy and non-celiac gluten/wheat sensitivity. Despite having in common the contact of the gastrointestinal mucosa with components of wheat and other cereals as a causative factor, these clinical entities have distinct pathophysiological pathways. [...] Read more.
Gluten-related disorders include distinct disease entities, namely celiac disease, wheat-associated allergy and non-celiac gluten/wheat sensitivity. Despite having in common the contact of the gastrointestinal mucosa with components of wheat and other cereals as a causative factor, these clinical entities have distinct pathophysiological pathways. In celiac disease, a T-cell mediate immune reaction triggered by gluten ingestion is central in the pathogenesis of the enteropathy, while wheat allergy develops as a rapid immunoglobulin E- or non-immunoglobulin E-mediated immune response. In non-celiac wheat sensitivity, classical adaptive immune responses are not involved. Instead, recent research has revealed that an innate immune response to a yet-to-be-defined antigen, as well as the gut microbiota, are pivotal in the development in this disorder. Although impairment of the epithelial barrier has been described in all three clinical conditions, its role as a potential pathogenetic co-factor, specifically in celiac disease and non-celiac wheat sensitivity, is still a matter of investigation. This article gives a short overview of the mucosal barrier of the small intestine, summarizes the aspects of barrier dysfunction observed in all three gluten-related disorders and reviews literature data in favor of a primary involvement of the epithelial barrier in the development of celiac disease and non-celiac wheat sensitivity. Full article
(This article belongs to the Special Issue Dietary Intake and Gluten-Associated Disease)
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