Stimulation of somatostatin secretion by 3-O-methylglucose in the perfused dog pancreas.

Abstract

3-O-methylglucose stimulates somatostatin secretion from the dog pancreas by a glucose-dependent and glucose-like effect. Therefore, it is possible that 3-O-methylglucose-stimulated somatostatin secretion is dependent on glucose metabolism. Somatostatin secretion from the endocrine pancreas is stimulated by glucose, glyceraldehyde, and dihydroxyacetone but not affected by fructose, galactose, or ribose. Whether the nonmetabolizable glucose analog, 3-O-methylglucose affects somatostatin secretion is, however, not known. We therefore, examined whether the glucose analog affects somatostatin secretion in the perfused dog pancreas. We found that when added to a medium containing 2.7 mM or 5.5 mM D-glucose, 3-O-methylglucose (10 mM) stimulated somatostatin secretion to the same extent as did an equivalent dose of D-glucose. The same stimulation was observed also with arginine at 2.5 mM in the perfusion medium. In contrast, 3-O-methylglucose did not stimulate somatostatin secretion in the absence of glucose in the perfusion medium. Mannoheptulose (5 mM), which inhibits glucose metabolism, completely blocked the secretion to both hexoses.