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

Conclusions: 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.

Background: 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.

Methods: We therefore, examined whether the glucose analog affects somatostatin secretion in the perfused dog pancreas.

Results: 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.