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Samuel Vaisrub, MD

JAMA. 1975;233(11):1195.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Whatever its physiologic role in normal glucose metabolism, glucagon now occupies center stage alongside insulin in the pathophysiologic drama of diabetes mellitus. Sometimes, it steals the show. The excess of glucagon, which invariably accompanies diabetic ketoacidosis, may play as important a part in causing gluconeogenesis, ketogenesis, and lipolysis as does the lack of insulin. Gerich and his associates¹ observed that ketoacidosis was delayed for 18 hours after insulin withdrawal in seven insulin-dependent diabetic patients whose glucagon secretion had been suppressed by somatostatin. By contrast, ketoacidosis supervened within ten hours of insulin deprivation when glucagon secretion was not inhibited. Clearly, in this stressful complication of diabetes, glucagon emerges as a villain whose misdeeds, it is hoped, will be prevented by somatostatin or its as yet untested analogs.

Hyperglucagonemia also occurs in stressful conditions that are related not to diabetes, but to shock. A number of investigators have published reports on . . . [Full Text PDF of this Article]

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