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SIMULATION OF THE NORMAL GLUCOPENIA-INDUCED DECLINE IN INSULIN PARTIALLY RESTORES THE GLUCAGON RESPONSE TO GLUCOPENIA IN ISOLATED PERFUSED PANCREATA OF STREPTOZOTOCIN-DIABETIC RATS

Veterans Administration Medical Center and The University of Texas Health Science Center at Dallas Dallas, Texas;
University of Perugia, School of Medicine Perugia, Italy.

Abstract

To determine if the loss of the glucagon response to glucopenia that follows destruction of beta cells is at least in part a consequence of the absence of the normal glucopenia-induced decline in insulin secretion, pancreata from insulin-requiring streptozotocin-diabetic rats were studied. In the absence of insulin, a reduction in perfusate glucose concentration from 150 to 25 mg/dl failed to elicit a rise in glucagon concentration. When insulin was co-perfused at 30 mU/ml, the estimated within-islet concentration of insulin under these circumstances, but discontinued during the glucopenic interval, reducing the insulin concentration in the pancreatic venous effluent from 26 mU/ml to <100 µU/ml, a prompt and significant rise in glucagon was observed until glucose and insulin levels were raised to their original concentrations. The rise in glucagon, which was approximately 25% of the normal response, did not occur when insulin concentration in the perfusate was maintained at 30 U/ml during the glucopenic period. Nor did it occur when insulin was perfused at 360 µU/ml and discontinued during the glucopenic period, thereby lowering insulin in the venous effluent from 300 µU/ml to 5 µU/ml. It is concluded that the decline in insulin from its normal concentrations within the islets makes a modest but significant contribution to the rise in glucagon that occurs during glucopenia.

Received July 30, 1985.

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