[Amelioration of glucose tolerance and correction of reactive hypoglycemias induced by intravenous calcium infusion cannot be explained by modifications in blood glucagon levels].

Glucagon is not involved in intravenous calcium-induced improvement in glucose tolerance nor in correction of reactive hypoglycemia. Recent investigations have shown that intravenous (IV) calcium infusion improved blood glucose values in patients with moderately impaired glucose tolerance, and suppressed hypoglycemia in patients with isolated reactive hypoglycemia. The aim of this study was to investigate the possibility that these changes were secondary to calcium induced alterations in glucagon (IRG) secretion. Four groups of subjects were studied: group 1: normal controls (n = 7); group 2: patients with isolated hypoglycemia (n = 9); group 3: patients with impaired glucose tolerance without reactive hypoglycemia (n = 9) and group 4: patients with impaired glucose tolerance and reactive hypoglycemia (n = 10). All patients were submitted in randomized order to two 5 hour oral glucose tolerance tests (OGTT, 75 g glucose), during a simultaneous infusion, either of saline or of calcium (calcium gluconate 36.3 mEq/5 h.), starting 30 minutes before the OGTT. In none of the groups did calcium infusion influence basal plasma IRG. In group 1 and 3, oral glucose significantly suppressed IRG, and during IV calcium infusion this suppression disappeared. In group 2, glucose ingestion resulted in a paradoxical increase in IRG both during saline and during calcium infusion. In group 4, oral glucose induced a significant drop in plasma IRG and a rebound rise during hypoglycemia, results which were unaffected by IV calcium infusion. These data suggest that glucagon is not involved in the alterations of blood glucose profiles during OGTT observed during intravenous calcium infusion.