Related Experiment Videos
Pancreatic hormone secretion in chronic pancreatitis without residual beta-cell function
S Larsen1, J Hilsted, B Tronier
1Medical Department F, Glostrup Hospital, University of Copenhagen, Denmark.
Acta Endocrinologica
|July 1, 1988
Summary
Patients with insulin-dependent diabetes from chronic pancreatitis show preserved pancreatic glucagon secretion and lower pancreatic polypeptide, but higher somatostatin levels compared to Type I diabetics and healthy individuals.
Area of Science:
- Endocrinology
- Gastroenterology
- Metabolic Disorders
Background:
- Insulin-dependent diabetes mellitus (Type I diabetes) is characterized by absolute insulin deficiency.
- Chronic pancreatitis can lead to secondary diabetes, often without residual beta-cell function.
- Hormonal dysregulation, including glucagon, pancreatic polypeptide, and somatostatin, is implicated in diabetes pathophysiology.
Purpose of the Study:
- To investigate and compare hormonal responses (glucagon, pancreatic polypeptide, somatostatin) in patients with diabetes secondary to chronic pancreatitis versus Type I diabetics and healthy controls.
- To determine if pancreatic glucagon secretion is preserved in diabetes associated with chronic pancreatitis.
- To explore the role of somatostatin in glucose regulation in these patient groups.
Main Methods:
- Hormonal responses to intravenous glucagon, intravenous arginine, and a mixed meal were measured.
- Study included 6 patients with diabetes secondary to chronic pancreatitis (no beta-cell function), 8 Type I diabetics (no beta-cell function), and 8 healthy subjects.
- Concentrations of glucagon, pancreatic polypeptide, and somatostatin were analyzed.
Main Results:
- No significant differences in glucagon response to arginine or meal were observed between the two diabetic groups.
- Patients with diabetes secondary to chronic pancreatitis exhibited significantly lower pancreatic polypeptide levels compared to Type I diabetics and healthy controls.
- Somatostatin concentrations were significantly higher in patients with diabetes secondary to chronic pancreatitis after all stimuli.
Conclusions:
- Pancreatic glucagon secretion appears to be preserved in insulin-dependent diabetes secondary to chronic pancreatitis, even without residual beta-cell function.
- Pancreatic glucagon deficiency is not absolute in this diabetic population.
- Elevated somatostatin levels in chronic pancreatitis-related diabetes may contribute to lower blood glucose levels.