Benzothiadiazine suppression of insulin release from normal and abnormal islet tissue in man.

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Abstract
The effects of trichlormethiazide and diazoxide on plasma levels of immuno-assayable insulin and blood levels of glucose were evaluated in 5 chlorpropamide-pretreated healthy subjects before and after administration of leucine and in 6 patients with functioning islet cell tumors. In the healthy subjects, the benzothiadiazine drugs produced elevations in blood glucose that were either associated with decreases or were not associated with increases in plasma insulin. Leucine-induced hypoglycemla and hyperinsulinemia were attenuated. The benzothiadiazine drugs did not decrease the hypoglycemic effect of exogenous insulin. In patients with insulin-producing pancreatic islet cell tumors, the benzothiadiazine drugs decreased hypoglycemia and hyperinsulinemia in the fasting state as well as postprandially. Glucose-induced insulin release was greatly diminished. These studies indicate that decreased insulin secretion as well as failure of appropriate increases in insulin secretion are involved in mechanisms by which trichlormethiazide and diazoxide induce hyperglycemia. They also suggest that these benzothiadiazines increase blood glucose by mechanisms that do not involve alterations in plasma isulin.