Abstract

Patients with type 1 diabetes (T1D) are at higher risk of celiac disease (CD). Recently, intestinal fatty acid binding protein (I-FABP) has been shown to be a serological biomarker of impaired intestinal barrier in CD. Thus, the aim of this study was to verify whether I-FABP could be an early marker of CD in pediatric T1D patients. I-FABP was measured in sera of patients with T1D (n = 156), active CD (n = 38), T1D with active CD (T1D-CD, n= 51), and age-matched healthy children (n = 55). Additionally, I-FABP was determined in T1D patients with negative CD serology at least one year before CD diagnosis (T1D-CD-1, n = 22), in CD patients on a gluten-free diet (CD-GFD, n = 36), and T1D-CD patients on GFD (T1D-CD-GFD, n = 39). Sera were tested using immunoenzymatic assay. Significantly increased levels of I-FABP were found in the T1D, active CD, and T1D-CD groups (1153 ± 665, 1104 ± 916, and 1208 ± 878, respectively) in comparison to healthy with controls (485 ± 416, p < 0.05). GFD induced a significant decrease in I-FABP levels in CD and T1D-CD groups (510 ± 492 and 548 ± 439, respectively). Interestingly, in T1D-CD-1 and T1D, I-FABP levels were comparable (833 ± 369 vs. 1153 ± 665), and significantly increased in relation to healthy controls and T1D-CD values on GFD. The results indicate that the epithelial barrier is disrupted in T1D patients independently of CD development; therefore, I-FABP cannot serve as an early marker of CD in T1D patients. Although GFD can improve epithelial recovery, the question remains as to whether GFD could exert beneficial effects on the intestinal barrier in early stages of T1D.

Highlights

  • Type 1 diabetes (T1D) is a multifactorial and complex autoimmune disease

  • intestinal fatty acid binding protein (I-FABP) Levels in Sera of T1D Patients without celiac disease (CD), Patients with Active CD, and Patients with T1DM and CD

  • There was a significant difference in I-FABP levels between the three study groups (T1D, active CD, and T1D-CD) and healthy controls: 1153 ± 665, 1104 ± 916, 1208 ± 878 vs. 485 ± 416 pg/mL, respectively; (p < 0.001) (Figure 1)

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Summary

Introduction

Type 1 diabetes (T1D) is a multifactorial and complex autoimmune disease. The co-diagnosis of CD affects from 2 to 16% of diabetic patients worldwide [1]. The human leukocyte antigen (HLA) analysis showed that haplotypes occurring in almost all patients with CD (HLA-DQ2 and HLA-DQ8) exist in the majority of patients with T1D, which confirms the hypothesis concerning the common genetic pathogenesis of both diseases [5,6]. Common genetic features of T1D and CD were documented in the genome-wide association study (GWAS), suggesting the role of impaired mucosal barrier function in the etiopathogenesis of both diseases [7]. In the altered gut barrier, non-competent intercellular junctions allow antigens, derived from the food or intestinal microbiota, to enter the circulation and activate the immune system into upregulated autoimmune responses [8]

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