The effect of experimental insulin deficiency on glucagon secretion

摘要: Abstract Suppression of pancreatic glucagon secretion by hyperglycemia is a characteristic normal alpha cell function. However, in diabetic subjects, plasma or high despite hyperglycemia. It seemed possible that the presence glucose its metabolites within might be essential for suppression secretion, and diabetes an intracellular deficiency secondary to insulin lack responsible nonsuppressibility. The present study was designed determine effect upon blockade metabolism experimental deficiency. Blockade induced dogs administration 2-deoxyglucose mannoheptulose. A striking rise observed accompanying hyperinsulinemia, which, case mannoheptulose, infusing crystalline insulin. To if also causes paradoxical hyperglucagonemia, were made severely alloxan. Fasting levels ranged from 3 22 times severe hyperglycemia, quickly restored insulin. Diabetes rats anti-insulin serum associated with significant elevation glucagon. diazoxide-induced did not increase dogs. It concluded does occur when blocked produced. suggested may insulin-requiring process without which hyperglycemic release cannot occur.