详细记录  
题名:Colonic delivery of docosahexaenoic acid improves impaired glucose tolerance via GLP-1 secretion and suppresses pancreatic islet hyperplasia in diabetic KK-A(y) mice.
作者:SHIDA T; KAMEI N; TAKEDA-MORISHITA M; ISOWA K; TAKAYAMA K;
来源:Int J Pharm. 2013 Jun 25;450(1-2):63-9. doi: 10.1016/j.ijpharm.2013.04.029. Epub [ IF= 0.00 ] ]
URL :10.1016/j.ijpharm.2013.04.029
日期:20130430
摘要:Glucagon-like peptide-1 (GLP-1) is an incretin hormone that regulates the insulin
secretion depending on blood glucose level. Recent studies show that the
unsaturated fatty acids can promote GLP-1 secretion from intestinal L-cells. We
have shown previously that docosahexaenoic acid (DHA) and eicosapentaenoic acid
(EPA) administered into a mouse closed intestinal loop, especially into the
colonic segment, stimulate GLP-1 and insulin secretion and have a hypoglycemic
effect, suggesting that DHA and EPA have potential as antidiabetic agents. The
present study examined the antidiabetic effect of DHA following long-term in vivo
delivery to the colon using normal ddY and diabetic KK-A(y) mice. The plasma
GLP-1 concentration of KK-A(y) mice increased after long-term DHA administration,
and this had a significant hypoglycemic effect. In contrast, although GLP-1
secretion in ddY mice tended to increase after DHA administration, blood glucose
concentration did not differ between vehicle- and DHA-treated ddY mice.
Immunostaining of the pancreas after long-term DHA administration showed that
continuous DHA treatment stimulated beta-cell apoptosis and accordingly
suppressed islet cell growth in KK-A(y) mice. Colon targeting of DHA may provide
a new strategy for improving impaired glucose tolerance in type 2 diabetes
mellitus by stimulating GLP-1 secretion, which may subsequently suppress the
compensatory hyperplasia of pancreatic islets.

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