Tungstate stimulates insulin release and inhibits somatostatin output in the perfused rat pancreas

In the rat pancreas, infusion of sodium-tungstate stimulates basal insulin release in a dose-dependent manner. We have studied tungstate's effects on the insulin secretion elicited by various B-cell secretagogues. Somatostatin output was also measured. The study was performed in the perfused pancreas isolated from normal or somatostatin-depleted pancreases as induced by cysteamine pre-treatment. In control rats, tungstate co-infusion (5 mM) potentiated the insulin secretory responses to glucose (2.7-fold; P < 0.01), arginine (2-fold; P < 0.01), exendin-4 (3-fold; P < 0.01), glucagon (4-fold; P < 0.05), and tolbutamide (2-fold; P < 0.01). It also inhibited the somatostatin secretory responses to glucose (90%; P < 0.01), arginine (95%; P < 0.01), glucagon (80%; P < 0.025), exendin-4 (80%; P < 0.05) and tolbutamide (85%; P < 0.01). In somatostatin-depleted pancreases, the stimulatory effect of tungstate on basal insulin secretion and its potentiation of arginine-induced insulin output were comparable to those found in control rats. Our observations suggest an amplifying effect of tungstate on a common step in the insulin stimulus/secretion coupling process, and would rule out a paracrine effect mediated by the inhibition of somatostatin secretion induced by this compound.