INFLUENCE OF RESIDUAL C-PEPTIDE SECRETION ON THE ARGININE-VASOPRESSINRESPONSE TO HYPOGLYCEMIA AND METOCLOPRAMIDE IN INSULIN-DEPENDENT DIABETES

Arginine vasopressin (AVP) hypersecretion in response to metoclopramid e or to insulin-induced hypoglycaemia has been described in type I dia betes mellitus. In the present study, we examined whether residual end ogenous insulin secretion may play a role in the control of this abnor mal AVP secretory pattern. For this purpose, 21 insulin-dependent diab etic men and 10 age- and weight-matched normal men were tested with MC P (20mg in an i.v. bolus). On a different occasion, subjects were test ed with insulin (0.15 IU kg(-1)). The diabetic patients were subdivide d into C-peptide negative patients (CpN, 11 patients without detectabl e endogenous pancreatic beta cell activity) (group I) and C-peptide po sitive patients (CpP, 10 patients with residual endogenous insulin sec retion) (group II). Experiments started after optimization of the meta bolic status of the diabetic men by 3 days of treatment with continuou s subcutaneous insulin infusion. The basal concentrations of AVP were similar in all groups. The administration of MCP induced a striking el evation in plasma AVP levels in the normal controls and in the diabeti c subjects of groups I and II. However, the AVP rise was significantly higher in group I and group II than in normal controls. Furthermore, group I diabetics showed higher AVP increments than group II. Insulin induced a similar hypoglycaemic nadir in all subjects at 30 min, even though the diabetic subjects of groups I and II had a delayed recovery in blood glucose levels. The hypoglycaemic pattern was similar in gro up I and II. Hypoglycaemia induced a striking AVP increase in the norm al controls. However, significantly higher AVP responses to hypoglycae mia were observed in the diabetic men of group I and group II than in the normal controls. Furthermore, group I diabetics showed higher AVP increments than group II. These data indicate that the hypothalamic-pi tuitary disorder affecting the AVP response to MCP and insulin-induced hypoglycaemia in well controlled type I diabetic men is inversely rel ated to residual p-cen activity.