Biphasic effect of somatostatin on oral glucose tolerance in maturity-onset diabetes

Oral glucose tolerance was examined in five maturity-onset diabetics during the infusion of somatostatin or saline. Somatostatin inhibited glucose-stimulated insulin release and reduced plasma glucagon by 50%–65%. The rise in plasma glucose after glucose ingestion was initially (at 30–120 min) reduced by somatostatin. However, beyond 3 hr, plasma glucose levels were 50–200 mg 100 ml higher, with somatostatin reaching concentrations at 6 hr that were twofold higher than those observed with saline ( p < 0.005). The degree of late glucose intolerance was inversely related to postglucose plasma insulin concentrations ( p < 0.01). These findings demonstrate a biphasic effect of somatostatin on oral glucose tolerance in maturity-onset diabetes. The exaggerated late hyperglycemia is related to suppression of insulin secretion. The initial blunting of postprandial hyperglycemia may reflect decreased carbohydrate absorption and/or hypoglucagonemia-mediated enhancement of glucose disposal.