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Journal of Diabetes Research
Volume 2016 (2016), Article ID 2424306, 11 pages
Research Article

Large Gliadin Peptides Detected in the Pancreas of NOD and Healthy Mice following Oral Administration

1The Bartholin Institute, Rigshospitalet, Copenhagen N, Denmark
2Clinical Biochemistry, Immunology & Genetics, Statens Serum Institut, Copenhagen S, Denmark
3The Hevesy Laboratory, DTU Nutech, Technical University of Denmark, Roskilde, Denmark
4Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, Prague 6, Czech Republic
5Enzyme Purification and Characterization, Novozymes A/S, Bagsværd, Denmark

Received 6 May 2016; Accepted 10 August 2016

Academic Editor: Marco Songini

Copyright © 2016 Susanne W. Bruun et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Gluten promotes type 1 diabetes in nonobese diabetic (NOD) mice and likely also in humans. In NOD mice and in non-diabetes-prone mice, it induces inflammation in the pancreatic lymph nodes, suggesting that gluten can initiate inflammation locally. Further, gliadin fragments stimulate insulin secretion from beta cells directly. We hypothesized that gluten fragments may cross the intestinal barrier to be distributed to organs other than the gut. If present in pancreas, gliadin could interact directly with the immune system and the beta cells to initiate diabetes development. We orally and intravenously administered 33-mer and 19-mer gliadin peptide to NOD, BALB/c, and C57BL/6 mice and found that the peptides readily crossed the intestinal barrier in all strains. Several degradation products were found in the pancreas by mass spectroscopy. Notably, the exocrine pancreas incorporated large amounts of radioactive label shortly after administration of the peptides. The study demonstrates that, even in normal animals, large gliadin fragments can reach the pancreas. If applicable to humans, the increased gut permeability in prediabetes and type 1 diabetes patients could expose beta cells directly to gliadin fragments. Here they could initiate inflammation and induce beta cell stress and thus contribute to the development of type 1 diabetes.