Summary Animals with NIDDM display abnormal glucose regulation of insulin secretion and biosynthesis. We tested reversibility of abnormal regulation by normoglycaemia using an islet transplantation technique. Inbred non-diabetic and neonatally STZ diabetic rats (n-STZ) were used. Transplantations insufficient to normalize the blood glucose levels (200 islets under kidney capsule) were performed from diabetic to normal (D-N) and from diabetic to diabetic (D-D), as well as from normal to normal (N-N) and from normal to diabetic (N-D) rats. Four weeks after transplantation, graft bearing kidneys were isolated and perfused with Krebs-Henseleit bicarbonate buffer to measure insulin secretion in response to 27.8 mmol/1 glucose and 10 mmol/1 arginine. Four weeks of normoglycaemia failed to restore glucose-induced insulin secretion from n-STZ islets (glucose induced increment: -1.7 + 2. 351-357]Key words Animal models NIDDM, insulin secretion, insulin mRNA, cytochrome b mRNA, islets of Langerhans.The neonatally STZ diabetic rat (n-STZ) is an animal model of NIDDM [review 1, 2]. In n-STZ insulin secretion is markedly abnormal at adult age despite only mild or moderate hyperglycaemia [1,2]. In particular, the insulin reponse to glucose is reduced out of proportion to the decrease in beta-cell mass. Responses to non-metabolised secretagogues, such as L-arginine or phosphodiesterase inhibitors, are however relatively preserved. This pattern of abnormalities bears resem-
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