The effects of repeated
injections of 75 U crude cholecystolinin-
pancreozymin (CCK-PZ) at increasing plateau
glucose concentrations achieved by
glucose infusion were studied in 15 controls, 8 chronic pancreatitics and 8 mild maturity onset diabetics. In control subjects CCK-PZ alone caused minor
insulin release but proportinally greater secretion with increasing
blood glucose concentrations.
Chronic pancreatitis patients who had normal responses to intravenous
glucose responded normally to the CCK-PZ but at significantly higher plateau
glucose levels. Diabetics had no response to IV
glucose boluses of 5 g or 10 g, but with
glucose infusions of 250-500 mg/min had almost normal
insulin responses to CCK-PZ. The responses to CCK-PZ plus
glucose were greater than either stimulus alone, indicating an interaction between these and the beta cell. These studies suggest that the gut homone-receptor in the beta cell is intact in
maturity onset diabetes and
chronic pancreatitis, whether the
glucose receptor is normal or defective. The
peptide-responsible in the crude CCK-PZ is not
secretin,
glucagon or
gut glucagon, but may be
gastric inhibitory polypeptide (GIP) since pure CCK-PZ has no insuli releasing properties.