The Controversy Concerning Counterregulatory Hormone Secretion: A Hypothesis for the Prevention of Diabetic Ketoacidosis?

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Abstract
Diabetic ketoacidosis is characterized by an excess secretion of counterregulatory hormones (glucagon, catecholamines, cortisol and growth hormone). Experimental evidence obtained in both diabetic man and animals suggests that elevation of the plasma concentration of these hormones is necessary to initiate excess hepatic production of ketone bodies. This increase in hepatic ketogenesis in concert with the inability of peripheral tissues to completely utilize ketone bodies results in clinical ketoacidosis. This hypothesis would suggest that pharmacologic control of excess counterregulatory hormone secretion would be a rational therapeutic modality to prevent diabetic ketoacidosis.