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Effects of some drugs on islet function in catfish
Indian Journal of Physiology and Pharmacology
|July 1, 1984
Summary
This study investigated how drugs affect catfish blood glucose and pancreatic islets. Drug treatments caused temporary blood sugar changes and visible changes in islet cells, which later regenerated.
Area of Science:
- Comparative physiology
- Endocrinology
- Aquatic toxicology
Background:
- Pancreatic islets are crucial for glucose regulation in vertebrates.
- Understanding drug-induced effects on fish islet cells is vital for aquaculture and ecotoxicology.
- Catfish serve as a valuable model for studying metabolic responses.
Purpose of the Study:
- To investigate the effects of glucose loading, alloxan, streptozotocin, and glybenclamide on blood glucose levels in catfish.
- To examine the associated bioptical cytopathological changes in pancreatic islet beta-cells.
- To assess the recovery of normoglycemic values and islet cell morphology post-treatment.
Main Methods:
- Administration of glucose, alloxan, streptozotocin, and glybenclamide to catfish.
- Monitoring of blood glucose levels over time.
- Histopathological examination of pancreatic islet tissues.
- Analysis of beta-cell changes, including regenerative activity and zinc content.
Main Results:
- Glucose loading induced dose-related hyperglycemia.
- Alloxan and streptozotocin caused transient hyperglycemic states with varying patterns.
- Glybenclamide induced hypoglycemia in normal fish but not in depancreatized fish.
- Pancreatic beta-cells showed histopathological changes and signs of regeneration; streptozotocin treatment led to zinc depletion.
Conclusions:
- Catfish exhibit distinct glycemic responses to various drug challenges.
- Pancreatic islet beta-cells demonstrate resilience and regenerative capacity following drug-induced stress.
- Drug-induced alterations in islet cell morphology and zinc content warrant further investigation.