By Stewart Wolf, Beatrice Bishop Berle (auth.), Stewart Wolf, Beatrice Bishop Berle (eds.)

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UNGER: Following a total pancreatectomy in some of these animals the glucagon levels went to The nitrogen sparing zero when insulin was given; they were responding in an exaggerated manner to effects of carbohydrates an amino acid infusion, in other words they were acting just like alloxanized animals. We made discriminatory assays of various parts of the gut looking for extra pancreatic glucagon. Finally this week we discovered a true glucagon different from GLI but indistinguishable from pancreatic glucagon.

UNGER: I suspect epinephrin because you can block it with adrenergic blocking agents, virtually or completely. DR. LEVINE: And, therefore, the epinephrin response is not due to low blood sugar either and, if so, then what is it due to? DR. UNGER: This must be centrally controlled. I do not know the mechanism. But the glucagon response to exercise closely resembles the response to stress in hypovolemic shock, whether due to infection or trauma -- this is what you see. Thus, insulin is fixed irrespective of glucose concentration and glucagon is high irrespective of glucose concentration.

Very elegant studies from Toronto by Cherrington and Vranic indicate that under similar circumstances glucose turnover rises up to 70% but glucose concentration stays relatively constant. Insulin changes alone could not achieve this; if insulin should rise without glucagon, glucose would fall. Moreover, the metabolic options provided by the bi-hormonal system would be lacking. It is, for example, possible for the liver to produce glucose without at the same time increasing lipolysis, because glucagon can increase glucose production without a decline in insulin.

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