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      The Impact of Diet Wheat Source on the Onset of Type 1 Diabetes Mellitus—Lessons Learned from the Non-Obese Diabetic (NOD) Mouse Model

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          Abstract

          Nutrition, especially wheat consumption, is a major factor involved in the onset of type 1 diabetes (T1D) and other autoimmune diseases such as celiac. While modern wheat cultivars possess similar gliadin proteins associated with the onset of celiac disease and T1D, alternative dietary wheat sources from Israeli landraces and native ancestral species may be lacking the epitopes linked with T1D, potentially reducing the incidence of T1D. The Non-Obese Diabetic (NOD) mouse model was used to monitor the effects of dietary wheat sources on the onset and development of T1D. The effects of modern wheat flour were compared with those from either T. aestivum, T. turgidum spp. dicoccoides, or T. turgidum spp. dicoccum landraces or a non-wheat diet. Animals which received wheat from local landraces or ancestral species such as emmer displayed a lower incidence of T1D and related complications compared to animals fed a modern wheat variety. This study is the first report of the diabetogenic properties of various dietary wheat sources and suggests that alternative dietary wheat sources may lack T1D linked epitopes, thus reducing the incidence of T1D.

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          Early infant feeding and risk of developing type 1 diabetes-associated autoantibodies.

          D. Huber, Ezio Bonifacio, Sandra Schmid … (2003)
          Dietary factors modifying type 1 diabetes mellitus (DM) risk have been proposed, but little is known if they trigger the islet autoimmunity that precedes clinical disease. To determine whether breastfeeding duration, food supplementation, or age at introduction of gluten-containing foods influences the risk of developing islet autoantibodies. Prospective natural history cohort study conducted from 1989 to 2003 in inpatient/outpatient clinics in Germany. The BABYDIAB study follows newborn children of parents with type 1 DM. Eligibility requirements were met in 1610 children. Blood samples were obtained at birth, age 9 months, 2, 5, and 8 years. Dropout rate was 14.4% by age 5 years. Breastfeeding data were obtained by prospective questionnaires (91% complete), and food supplementation data were obtained by family interview (72% for food supplementation and 80% for age of gluten introduction). Development of islet autoantibodies (insulin, glutamic acid decarboxylase, or IA-2 antibodies) in 2 consecutive blood samples. Life-table islet autoantibody frequency was 5.8% (SE, 0.6%) by age 5 years. Reduced total or exclusive breastfeeding duration did not significantly increase the risk of developing islet autoantibodies. Food supplementation with gluten-containing foods before age 3 months, however, was associated with significantly increased islet autoantibody risk (adjusted hazard ratio, 4.0; 95% confidence interval, 1.4-11.5; P =.01 vs children who received only breast milk until age 3 months). Four of 17 children who received gluten foods before age 3 months developed islet autoantibodies (life-table 5-year risk, 24%; SE, 10%). All 4 children had the high-risk DRB1*03/04,DQB1*0302 genotype. Early exposure to gluten did not significantly increase the risk of developing celiac disease-associated autoantibodies. Children who first received gluten foods after age 6 months did not have increased risks for islet or celiac disease autoantibodies. Ensuring compliance to infant feeding guidelines is a possible way to reduce the risk of development of type 1 DM autoantibodies.
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            Timing of initial cereal exposure in infancy and risk of islet autoimmunity.

            Henry Erlich, Marian Rewers, Katherine J. Barriga … (2003)
            Dietary exposures in infancy have been implicated, albeit inconsistently, in the etiology of type 1 diabetes mellitus (DM). To examine the association between cereal exposures in the infant diet and appearance of islet autoimmunity (IA). Birth cohort study conducted from 1994 to 2002 with a mean follow-up of 4 years. Newborn screening for HLA was done at St Joseph's Hospital in Denver, Colo. First-degree relatives of type 1 DM individuals were recruited from the Denver metropolitan area. We enrolled 1183 children at increased type 1 DM risk, defined as either HLA genotype or having a first-degree relative with type 1 DM, at birth and followed them prospectively. We obtained exposure and outcome measures for 76% of enrolled children. Participants had variable lengths of follow-up (9 months to 9 years). Blood draws for the detection of insulin autoantibody, glutamic acid decarboxylase autoantibody, or IA-2 autoantibody were performed at 9, 15, and 24 months and annually thereafter. Children with IA (n = 34) were defined as those testing positive for at least 1 of the autoantibodies on 2 or more consecutive visits and who tested positive or had diabetes on their most recent visit. Children initially exposed to cereals between ages 0 and 3 months (hazard ratio [HR], 4.32; 95% confidence interval [CI], 2.0-9.35) and those who were exposed at 7 months or older (HR, 5.36; 95% CI, 2.08-13.8) had increased hazard of IA compared with those who were exposed during the fourth through sixth month, after adjustment for HLA genotype, family history of type 1 DM, ethnicity, and maternal age. In children who were positive for the HLA-DRB1*03/04,DQB8 genotype, adjusted HRs were 5.55 (95% CI, 1.92-16.03) and 12.53 (95% CI, 3.19-49.23) for initial cereal exposure between ages 0 to 3 months and at 7 months or older, respectively. There may be a window of exposure to cereals in infancy outside which initial exposure increases IA risk in susceptible children.
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              Celiac disease and risk of subsequent type 1 diabetes: a general population cohort study of children and adolescents.

              Polly S. Montgomery, Jonas F. Ludvigsson, Anders Ekbom … (2006)
              Earlier studies suggest that children with type 1 diabetes are more likely to have a subsequent diagnosis of celiac disease. However, research is sparse on the risk of subsequent type 1 diabetes in individuals with celiac disease. We sought to determine the risk of subsequent type 1 diabetes diagnosed before the age of 20 years in children and adolescents with celiac disease in a national, general population-based cohort. We identified 9,243 children with a diagnosis of celiac disease in the Swedish national inpatient register between 1964 and 2003. We then identified five reference individuals matched at time of diagnosis for age, calendar year, sex, and county (n = 45,680). Only individuals with >1 year of follow-up after study entry (diagnosis of celiac disease) were included in the analyses. Celiac disease was associated with a statistically significantly increased risk of subsequent type 1 diabetes before age 20 years (hazard ratio 2.4 [95% CI 1.9-3.0], P < 0.001). This risk increase was seen regardless of whether celiac disease was first diagnosed between 0 and 2 (2.2 [1.7-2.9], P < 0.001) or 3 and 20 (3.4 [1.9-6.1], P < 0.001) years of age. Individuals with prior celiac disease were also at increased risk of ketoacidosis or diabetic coma before the age of 20 years (2.3 [1.4-3.9], P = 0.001). Children with celiac disease are at increased risk of subsequent type 1 diabetes. This risk increase is low considering that 95% of individuals with celiac disease are HLA-DQ2 positive.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Nutrients
                Journal ID (iso-abbrev): Nutrients
                Journal ID (publisher-id): nutrients
                Title: Nutrients
                Publisher: MDPI
                ISSN (Electronic): 2072-6643
                Publication date (Electronic): 10 May 2017
                Publication date Collection: May 2017
                Volume: 9
                Issue: 5
                Electronic Location Identifier: 482
                Affiliations
                [1 ]Eastern Regional Research and Development Center, Judea Center, Kiryat Arba 90100, Israel; yludmila@ 123456post.bgu.ac.il (L.Y.); abudovsky@ 123456gmail.com (A.B.)
                [2 ]Department of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, Beer Sheva 84990, Israel; boriskh83@ 123456gmail.com (B.K.); sbs@ 123456bgu.ac.il (S.B.-S.)
                [3 ]Institute of Plant Sciences, ARO-Volcani Center, Rishon LeZion 50250, Israel; vcjosh@ 123456volcani.agri.gov.il
                [4 ]Siap Laboratory, Rehovot 76267, Israel; siap.013.lab@ 123456gmail.com
                [5 ]Department of Information Science and Systems, Morgan State University, Baltimore, MD 21251, USA; maxim.bushuev@ 123456morgan.edu
                [6 ]Scheller College of Business at Georgia Tech, Atlanta, GA 30308, USA; tatiana.rudchenko@ 123456scheller.gatech.edu
                Author notes
                [* ]Correspondence: jonathangorelick@ 123456gmail.com ; Tel.: +972-52-605-1332
                Article
                Publisher ID: nutrients-09-00482
                DOI: 10.3390/nu9050482
                PMC ID: 5452212
                PubMed ID: 28489059
                SO-VID: 6c599bda-9500-4e53-ac30-be5b2cb6ad65
                Copyright © © 2017 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 26 January 2017
                Date accepted : 25 April 2017
                Categories
                Subject: Article

                ScienceOpen disciplines: Nutrition & Dietetics
                Keywords: type 1 diabetes mellitus,wheat,non-obese diabetic (nod) mouse,emmer,triticum dicoccoides
                Data availability:
                ScienceOpen disciplines: Nutrition & Dietetics
                Keywords: type 1 diabetes mellitus, wheat, non-obese diabetic (nod) mouse, emmer, triticum dicoccoides

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