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Endocrine pancreatic morphology and function in exocrine insufficiency in rats
The American Journal of Physiology
|August 1, 1987
Summary
Exocrine pancreatic insufficiency in rats impairs glucose-stimulated insulin release from the pancreas, despite intact islets. This suggests a link between exocrine function and beta-cell responsiveness, impacting glucose tolerance.
Area of Science:
- Endocrinology
- Gastroenterology
- Physiology
Background:
- Exocrine pancreatic insufficiency (EPI) is a condition characterized by the inability of the pancreas to produce or secrete sufficient digestive enzymes.
- The pancreas has both exocrine and endocrine functions, with the islets of Langerhans responsible for hormone production like insulin.
- The relationship between exocrine pancreatic function and endocrine pancreatic function, particularly insulin secretion, is not fully understood.
Purpose of the Study:
- To investigate the impact of induced exocrine pancreatic insufficiency on insulin secretion and glucose tolerance in rats.
- To determine if exocrine atrophy affects the structure and cell composition of the islets of Langerhans.
- To assess the dynamic insulin response in isolated perfused pancreases and glucose tolerance in vivo.
Main Methods:
- Exocrine pancreatic insufficiency was induced in rats using oleic acid injection into the pancreatic duct.
- Histological analysis was performed to assess exocrine tissue reduction and islet cell distribution.
- Insulin release was measured from isolated perfused pancreases stimulated by glucose and arginine, and oral and intravenous glucose tolerance tests were conducted in vivo.
Main Results:
- Induction of EPI led to a 98% reduction in exocrine pancreatic tissue, while islets of Langerhans remained intact.
- In isolated perfused pancreases, glucose- and arginine-stimulated insulin release was significantly reduced in rats with EPI.
- Despite reduced insulin secretion in vitro, oral and intravenous glucose tolerance tests in vivo showed only a slight impairment in glucose tolerance, with no significant differences in serum glucose or insulin levels compared to controls.
Conclusions:
- Induced exocrine pancreatic insufficiency in rats leads to significant reductions in stimulated insulin release from the pancreas.
- The findings suggest a functional link between the exocrine pancreas and the endocrine pancreas's ability to secrete insulin.
- While in vitro studies show impaired insulin release, in vivo glucose tolerance tests reveal a less pronounced effect, indicating potential compensatory mechanisms or limitations of the models used.