The Role of Gluten in Celiac Disease and Type 1 Diabetes

被引:51
作者
Serena, Gloria [1 ,2 ,3 ]
Camhi, Stephanie [1 ,2 ]
Sturgeon, Craig [1 ,2 ,3 ]
Yan, Shu [1 ,2 ]
Fasano, Alessio [1 ,2 ]
机构
[1] Massachusetts Gen Hosp, Ctr Celiac Res, Mucosal Immunol & Biol Res Ctr, Boston, MA 02114 USA
[2] Massachusetts Gen Hosp Children, Div Pediat Gastroenterol & Nutr, Boston, MA 02114 USA
[3] Univ Maryland, Sch Med, Grad Program Life Sci, Baltimore, MD 21201 USA
关键词
celiac disease; type; 1; diabetes; gluten; INTESTINAL PERMEABILITY; ISLET AUTOIMMUNITY; TISSUE TRANSGLUTAMINASE; ENTEROVIRUS INFECTIONS; MICROBIOTA COMPOSITION; TYROSINE PHOSPHATASE; DIETARY INTERVENTION; IMMUNE-RESPONSE; WHEAT GLUTEN; RISK-FACTORS;
D O I
10.3390/nu7095329
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Celiac disease (CD) and type 1 diabetes (T1D) are autoimmune conditions in which dietary gluten has been proven or suggested to play a pathogenic role. In CD; gluten is established as the instigator of autoimmunity; the autoimmune process is halted by removing gluten from the diet; which allows for resolution of celiac autoimmune enteropathy and subsequent normalization of serological markers of the disease. However; an analogous causative agent has not yet been identified for T1D. Nevertheless; the role of dietary gluten in development of T1D and the potentially beneficial effect of removing gluten from the diet of patients with T1D are still debated. In this review; we discuss the comorbid occurrence of CD and T1D and explore current evidences for the specific role of gluten in both conditions; specifically focusing on current evidence on the effect of gluten on the immune system and the gut microbiota.
引用
收藏
页码:7143 / 7162
页数:20
相关论文
共 111 条
[1]   Perinatal risk factors increase the risk of being affected by both type 1 diabetes and coeliac disease [J].
Adlercreutz, Emma H. ;
Wingren, Carl Johan ;
Vincente, Raquel P. ;
Merlo, Juan ;
Agardh, Daniel .
ACTA PAEDIATRICA, 2015, 104 (02) :178-184
[2]   In vivo antigen challenge in celiac disease identifies a single transglutaminase-modified peptide as the dominant A-gliadin T-cell epitope [J].
Anderson, RP ;
Degano, P ;
Godkin, AJ ;
Jewell, DP ;
Hill, AVS .
NATURE MEDICINE, 2000, 6 (03) :337-342
[3]  
[Anonymous], 2012, DIABETES CARE, V35, pS11, DOI [10.2337/dc12-s004, 10.2337/dc35-S011]
[4]   Celiac disease pathogenesis:: The proinflammatory cytokine network [J].
Antonio Garrote, Jose ;
Gomez-Gonzalez, Emma ;
Bernardo, David ;
Arranz, Eduardo ;
Chirdo, Fernando .
JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION, 2008, 47 :S27-S32
[5]   Type 1 diabetes [J].
Atkinson, Mark A. ;
Eisenbarth, George S. ;
Michels, Aaron W. .
LANCET, 2014, 383 (9911) :69-82
[6]   In vitro-deranged intestinal immune response to gliadin in type 1 diabetes [J].
Auricchio, R ;
Paparo, F ;
Maglio, M ;
Franzese, A ;
Lombardi, F ;
Valerio, G ;
Nardone, G ;
Percopo, S ;
Greco, L ;
Troncone, R .
DIABETES, 2004, 53 (07) :1680-1683
[7]   IDENTIFICATION OF THE 64K AUTOANTIGEN IN INSULIN-DEPENDENT DIABETES AS THE GABA-SYNTHESIZING ENZYME GLUTAMIC-ACID DECARBOXYLASE [J].
BAEKKESKOV, S ;
AANSTOOT, HJ ;
CHRISTGAU, S ;
REETZ, A ;
SOLIMENA, M ;
CASCALHO, M ;
FOLLI, F ;
RICHTEROLESEN, H ;
CAMILLI, PD .
NATURE, 1990, 347 (6289) :151-156
[8]   Frequent delay of coeliac disease diagnosis in symptomatic patients with type 1 diabetes mellitus: Clinical and genetic characteristics [J].
Bakker, Sjoerd F. ;
Tushuizen, Maarten E. ;
Stokvis-Brantsma, Wilhelmina H. ;
Aanstoot, Henk J. ;
Winterdijk, Per ;
van Setten, Petra A. ;
von Blomberg, Boudewina M. ;
Mulder, Chris J. ;
Simsek, Suat .
EUROPEAN JOURNAL OF INTERNAL MEDICINE, 2013, 24 (05) :456-460
[9]   Type 1 diabetes and celiac disease in adults: glycemic control and diabetic complications [J].
Bakker, Sjoerd F. ;
Tushuizen, Maarten E. ;
von Blomberg, Mary E. ;
Mulder, Chris J. ;
Simsek, Suat .
ACTA DIABETOLOGICA, 2013, 50 (03) :319-324
[10]   A POLYMORPHIC LOCUS NEAR THE HUMAN INSULIN GENE IS ASSOCIATED WITH INSULIN-DEPENDENT DIABETES-MELLITUS [J].
BELL, GI ;
HORITA, S ;
KARAM, JH .
DIABETES, 1984, 33 (02) :176-183