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Somatostatin secretion in diabetic rabbits
Metabolism: Clinical and Experimental
|May 1, 1982
Summary
Diabetic rabbits exhibit hyperglycemia due to a decrease in beta cell mass and a severe defect in insulin release, despite normal somatostatin-like immunoreactivity (SLI) and glucagon levels.
Area of Science:
- Endocrinology
- Metabolic Disorders
- Animal Models
Background:
- Spontaneous hyperglycemia in New Zealand white rabbits is characterized by low insulin levels.
- This rabbit model offers a unique opportunity to study diabetes pathogenesis.
- Understanding beta cell function in this model is crucial for diabetes research.
Purpose of the Study:
- To investigate glucose, somatostatin-like immunoreactivity (SLI), and glucagon levels in diabetic rabbits.
- To assess insulin and SLI content in pancreatic islets of diabetic and normal rabbits.
- To characterize the defect in insulin release in this spontaneous diabetes model.
Main Methods:
- Portal vein blood samples were collected during glucose infusion in diabetic and normal rabbits.
- Glucose, SLI, and glucagon concentrations were measured.
- Insulin and SLI were extracted and quantified from isolated pancreatic islets.
Main Results:
- Diabetic rabbits showed a moderate decrease in insulin content per islet, but not per microgram of protein.
- SLI content per islet was similar to controls, but increased per microgram of protein.
- Portal and peripheral plasma concentrations of SLI and glucagon were comparable between diabetic and control rabbits.
Conclusions:
- The studied rabbit colony develops diabetes with reduced beta cell mass.
- The remaining beta cells in these diabetic rabbits have a significant defect in insulin secretion.
- This model is valuable for studying beta cell dysfunction in diabetes.