IMPAIRED 2ND-PHASE INSULIN-RESPONSE OF DIABETES-PRONE C57BL/6J MOUSE ISLETS

被引:24
作者
WENCEL, HE
SMOTHERS, C
OPARA, EC
KUHN, CM
FEINGLOS, MN
SURWIT, RS
机构
[1] DUKE UNIV, MED CTR, DEPT PSYCHIAT, DURHAM, NC 27708 USA
[2] DUKE UNIV, MED CTR, DEPT MED, DURHAM, NC 27708 USA
[3] DUKE UNIV, MED CTR, DEPT SURG, DURHAM, NC 27708 USA
[4] DUKE UNIV, MED CTR, DEPT PHARMACOL, DURHAM, NC 27708 USA
关键词
NIDDM; INSULIN SECRETION; MOUSE MODEL;
D O I
10.1016/0031-9384(95)00022-B
中图分类号
B84 [心理学];
学科分类号
04 ; 0402 ;
摘要
The C57BL/6J mouse develops obesity and diabetes in response to a high-fat, high-simple carbohydrate diet. To determine the dynamics of glucose-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 control 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 animals fed a diabetogenic diet. It is suggested that a latent deficiency of second phase insulin release may contribute to the development of the diet-induced syndrome in this model.
引用
收藏
页码:1215 / 1220
页数:6
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