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Genetic Variants in GLUT14 Gene Enhance Susceptibility to Inflammatory Bowel Disease
Author(s) -
amir shaghaghi mandana,
Bernstein Charles,
Eck peter
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.591.3
Subject(s) - inflammatory bowel disease , ulcerative colitis , genotype , medicine , gastroenterology , immunology , allele , crohn's disease , population , genetic predisposition , disease , biology , genetics , gene , environmental health
Oxidative stress is implicated in the initiation and progression of inflammatory bowel disease (IBD). Dehydroascorbic acid (DHA) is actively imported into cells via glucose transporters (GLUTs) and contributes to the vitamin C antioxidant cycle. This study aimed to determine if the recently indentified GLUT 14 gene is associated with susceptibility to IBD and the clinical phenotype. Participants in the population‐based Manitoba IBD Cohort Study were phenotyped using the Montreal classification. Genomic DNA samples from persons with Crohn's disease (CD, n=162) and ulcerative colitis (UC, n=149) and ethnically matched controls (n=142) were genotyped for eight GLUT 14 polymorphisms, using TaqMan assays. Logistic regression was used to determine the case‐control association of genotypes for each polymorphism with CD, UC, and overall IBD risks. Genotype‐phenotype associations were tested by multinomial logistic regression, using SAS software 9.2. Variant rs2889504‐A was associated with increased susceptibility to UC, CD, and overall IBD (OR: 3.60, 95% CI: 1.95‐6.64; OR: 4.68, 95% CI: 2.78, 8.50; OR: 4.14; 95% CI: 2.37‐7.22 respectively). The rs10846086‐G allele was associated with an approximated 3‐fold increased risk of UC, CD, and IBD. Variant rs12815313‐T was associated with increased susceptibility to CD and overall IBD OR: 2.12, 95% CI: 1.33‐3.36; OR: 1.85, 95% CI 2.41 (1.24‐2.77; respectively). These findings provide a novel opportunity toward individualized nutritional therapy for patients carrying the disease‐associated genotype. Further studies are now needed to elucidate the pathogenetic mechanism. (Supported by Peter Eck's Canada Research Chair)