DEFECTIVE GLUCOSE-STIMULATED INSULIN RELEASE FROM PERIFUSED ISLETS OFC57BL 6J MICE/

Citation
Sk. Lee et al., DEFECTIVE GLUCOSE-STIMULATED INSULIN RELEASE FROM PERIFUSED ISLETS OFC57BL 6J MICE/, Pancreas, 11(2), 1995, pp. 206-211
Citations number
28
Categorie Soggetti
Endocrynology & Metabolism",Physiology
Journal title
ISSN journal
08853177
Volume
11
Issue
2
Year of publication
1995
Pages
206 - 211
Database
ISI
SICI code
0885-3177(1995)11:2<206:DGIRFP>2.0.ZU;2-Y
Abstract
Previous work has shown that the C57BL/6J (BL/6) mouse strain develops type 2 diabetes after being fed a high-fat, high-simple carbohydrate (HFHSC) diet. In contrast, the AJ mouse strain does not. The aim of th e present study was to determine if differences in the insulin secreto ry characteristics of isolated perifused islets of these animals could help explain why the BL/6 mouse develops diet-induced diabetes. Insul in secretion was assessed as mean integrated area under the curve duri ng 20 min of stimulation with 27.7 mM glucose or 5 mM lauric acid. We found that both glucose- and laurate-stimulated insulin secretions wer e significantly less in euglycemic BL/6 mice than in the euglycemic AJ mice. The defect in insulin response to glucose, but not laurate, in islets from the BL/6 mouse was exacerbated when the animals were fed t he HFHSC diet. These data suggest that the BL/6 mouse has a defective insulin response to glucose, which is exacerbated by a diabetogenic di et.