详细记录  
题名: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.
作者:DALL M; CALLOE K; HAUPT-JORGENSEN M; LARSEN J; SCHMITT N; JOSEFSEN K; BUSCHARD K;
来源:PLoS One. 2013 Jun 13;8(6):e66474. doi: 10.1371/journal.pone.0066474. Print 2013. [ IF= 4.09 ] ]
URL :10.1371/journal.pone.0066474
日期:20130702
摘要:In non-obese diabetic (NOD) mice, diabetes incidence is reduced by a gluten-free
diet. Gluten peptides, such as the compound gliadin, can cross the intestinal
barrier and may directly affect pancreatic beta cells. We investigated the
effects of enzymatically-digested gliadin in NOD mice, INS-1E cells and rat
islets. Six injections of gliadin digest in 6-week-old NOD mice did not affect
diabetes development, but increased weight gain (20% increase by day 100). In
INS-1E cells, incubation with gliadin digest induced a dose-dependent increase in
insulin secretion, up to 2.5-fold after 24 hours. A similar effect was observed
in isolated rat islets (1.6-fold increase). In INS-1E cells, diazoxide reduced
the stimulatory effect of gliadin digest. Additionally, gliadin digest was shown
to decrease current through KATP-channels. A specific gliadin 33-mer had a
similar effect, both on current and insulin secretion. Finally, INS-1E incubation
with gliadin digest potentiated palmitate-induced insulin secretion by 13%
compared to controls. Our data suggest that gliadin fragments may contribute to
the beta-cell hyperactivity observed prior to the development of type 1 diabetes.

================  评  论  部  分=================

重要性:
分类:(参照 Faculty of 1000 的分类体系)


评语:

评论密码:   返回前页  [全部]