The C57BL/6J mouse develops obesity and diabetes in response to a high
-fat, high-simple carbohydrate diet. To determine the dynamics of gluc
ose-induced insulin release in this animal model of NIDDM, we studied
the acute insulin response to glucose of perifused islets in C57BL/6J
(diabetes-prone) and A/J (diabetes-resistant) mice fed a normal contro
l diet and of others fed a diabetogenic diet. The insulin response of
normal C57BL/6J islets was almost monophasic, with a deficiency in the
second phase during high glucose stimulation when compared to that of
A/J control islets. The defect in C57BL/6J mice was exaggerated in an
imals fed a diabetogenic diet. It is suggested that a latent deficienc
y of second phase insulin release may contribute to the development of
the diet-induced syndrome in this model.