Large Gliadin Peptides Detected in the Pancreas of NOD and Healthy Mice following Oral Administration
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388963%3A_____%2F16%3A00467362" target="_blank" >RIV/61388963:_____/16:00467362 - isvavai.cz</a>
Result on the web
<a href="https://www.hindawi.com/journals/jdr/2016/2424306/" target="_blank" >https://www.hindawi.com/journals/jdr/2016/2424306/</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1155/2016/2424306" target="_blank" >10.1155/2016/2424306</a>
Alternative languages
Result language
angličtina
Original language name
Large Gliadin Peptides Detected in the Pancreas of NOD and Healthy Mice following Oral Administration
Original language description
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.
Czech name
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Czech description
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Classification
Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
CC - Organic chemistry
OECD FORD branch
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Result continuities
Project
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Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2016
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Journal of Diabetes Research
ISSN
2314-6745
e-ISSN
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Volume of the periodical
2016
Issue of the periodical within the volume
Aug
Country of publishing house
US - UNITED STATES
Number of pages
11
Pages from-to
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UT code for WoS article
000387688700001
EID of the result in the Scopus database
2-s2.0-84992348153