The primary pathogenetic role of insulin lack in the hyperglycemia and ketoacidosis of diabetes, so long taken for granted, has been recently disputed by a number of investigators. Unger's group1 and others have marshalled experimental evidence to ascribe an essential role to glucagon excess in these homeostatic disturbances. Particularly impressive was the observation by Gerich et al2 that somatostatin, which inhibits glucagon as well as insulin, delayed ketoacidosis even when insulin was not given for 18 hours. As a corollary to these experimental findings emerged the concept of diabetes as a bihormonal disorder dependent not only on insulin deficiency but also on glucagon excess. The latter, it was hoped, would be controlled by somatostatin when the hormone became available for general use.
The theoretical and practical implications of the focus on glucagon are currently undergoing critical reappraisal. Barnes et al3 observed no substantial change in plasma glucagon
Vaisrub S. The Primacy of Insulin. JAMA. 1976;236(11):1274–1275. doi:10.1001/jama.1976.03270120050030
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