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.