Rapid endoportal injections of glucagon in a dose (1 μg.) which does not elevate thearterial glucagon concentration beyond the physiologic range caused a prompt rise in both mean arterial glucose and pancreaticoduodenal insulin concentration to a peak six minutes later. Hyperglycemia of similar magnitude produced by intravenous glucose infusion failed to elicit, as great a rise in insulin release.
With smaller doses of glucagon a more variable response was observed; however, in some dogs doses of glucagon which were too small to cause a significant change in arterial glucagon concentration did cause a rise in both glucose and insulin levels.
It is concluded that glucagon administered in physiologic doses via-the portarvenous system elicits a greater rise in insulin release than can be attributed to the concomitant hyperglycemia and, as suggested by others, does possess the qualifications of a potentiator of insulin secretion.