Selective Defect in Insulin Release in One Form of Spontaneous Laboratory Diabetes

THE New Zealand obese (NZO) mouse is characterized by genetically determined obesity, accompanied by insulin resistance, glucose intolerance and hyperinsulinaemia^1–4. The pattern of insulin release in response to stimuli has not been described. In the experiments reported here, a marked functional abnormality of the islets of Langerhans in vivo was observed, with no response of plasma insulin to glucose, glucagon and tolbutamide but a greatly exaggerated response to arginine. This observation of a selective defect of islet function not only has important implications concerning the normal physiology of insulin release but may also aid in understanding the evolution of the abnormalities of islet cell function in human diabetes⁵.