Gliadin Fragments and a Specific Gliadin 33-mer Peptide Close KATP Channels and Induce Insulin Secretion in INS-1E Cells and Rat Islets of Langerhans
Gliadin
Pancreatic Islets
Diazoxide
NOD mice
DOI:
10.1371/journal.pone.0066474
Publication Date:
2013-06-13T17:13:58Z
AUTHORS (7)
ABSTRACT
In non-obese diabetic (NOD) mice, diabetes incidence is reduced by a gluten-free diet. Gluten peptides, such as the compound gliadin, can cross intestinal barrier and may directly affect pancreatic beta cells. We investigated effects of enzymatically-digested gliadin in NOD INS-1E cells rat islets. Six injections digest 6-week-old mice did not development, but increased weight gain (20% increase day 100). cells, incubation with induced dose-dependent insulin secretion, up to 2.5-fold after 24 hours. A similar effect was observed isolated islets (1.6-fold increase). diazoxide stimulatory digest. Additionally, shown decrease current through KATP-channels. specific 33-mer had effect, both on secretion. Finally, potentiated palmitate-induced secretion 13% compared controls. Our data suggest that fragments contribute beta-cell hyperactivity prior development type 1 diabetes.
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