Prostaglandins, the Glucoreceptor, and Diabetes

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Abstract
The "glucoreceptor" hypothesis has evolved in large part from one of the few surviving generalizations about diabetes mellitus. Patients with this disorder do not respond appropriately to glucose signals. For example, those with hyperglycemia during fasting do not have first-phase insulin secretion (the acute insulin response) after an intravenous glucose challenge.1 Suppression of growth hormone2 and glucagon3 by glucose is impaired in diabetics, and taste buds may have a subnormal perception of glucose molecules.4 Hepatic glucose output, normally suppressed by increments in circulating glucose, remains high in diabetics despite the presence of hyperglycemia.5 A failure to respond to glucose signals . . .