Abstract
The early (10 minute) immunoreactive insulin release in response to various stimuli
in patients with severe pancreatic exocrine insufficiency was compared to controls.
The mean 10 minute incremental area of the response to combined glucose, glucagon
and tolbutamide was severely reduced in patients (728 ± 287.7 vs 2714 ± 479.9 µU minutes;
p < 0.0025).
Mean insulin responses to oral glucose were similar in patients and controls, but
the insulin response to intravenous glucose was absent in 4 of 6 patients (patients
79.0 ±51.2 vs controls 874 ± 171.9 µU/minutes; p < 0.0025).
All patients retained some insulin responsiveness to intravenous arginine.
Intravenous secretin produced an insulin response in all patients (57.6 ± 17.6 and
controls 220± 70.8 µU minutes; p < 0.05).
Cholecystokinin pancreozymin (CCK-PZ) produced an insulin response in 5 of 6 patients
(38± 17.9 vs 158 ± 30.7 µU minutes; p < 0.005).
It is concluded that in chronic pancreatitis -
(1) the beta cell glucose sensitive mechanism may be defective, while the glucose-stimulated
pathway of the entero-insular axis is maintained;
(2) Arginine-induced insulin secretion is mediated differently from the intravenous
glucose-induced response;
(3) insulin responses to Secretin and CCK-PZ are retained, which may partially explain
the insulin response to oral glucose.
Key words
Chronic Pancreatitis - Oral Glucose - Intravenous Glucose - Arginine - Secretin -
Cholecystokinin - Pancreozymin - Entero-Insular Axis - Insulin
