Homeira Zardouz, Saleh Zahedi Asl, Mohammad Kazem Gharib Naseri,
Volume 5, Issue 4 (17 2006)
Abstract
Background: Regarding the adverse effect of stress on glycemic control in type 2 diabetic patients, the present study investigates the function of Glibenclamide on insulin release from β cells of rat pancreatic islets, subsequent to chronic psychological stress exposure.
Methods: In this study 30 male Wistar rats were divided into equal groups of control and experiment (5 groups). Four different restraint stressors with random sequence were used 1h twice daily for 15 and 30 days. 24 hours after the last stress session, static insulin secretion from isolated pancreatic islets of each animal were evaluated in the presence of 5.6, 8.3 and 16.7 mM glucose. Also insulin release in response to 5.6 mM glucose in the presence of 10 μM Glibenclamide was evaluated.
Results: The insulin release from isolated islets of the stress experienced animals was significantly increased only on the 30th day as compared to the control animals. In the experiment group, insulin release from the islets in the presence of 5.6 mM glucose alone was significantly increased on the 15th and 30th days as compared to the first day. However, in the control group there was no significant increase in insulin release at the similar conditions. In contrast to the control group, insulin release in response to 5.6 mM glucose in the presence of 10 μM Glibenclamide revealed no significant difference in the experiment group on the 1st 15th and 30th days as compared to the insulin release in the presence of 5.6 mM glucose alone. Insulin release from the isolated islets exposed to 5.6 mM glucose in the presence of 10 μM Glibenclamide, on different experimental days was not significantly different between the control and experiment groups.
Conclusion: According to the results of this study, it appears that chronic psychological stress decreases the responsiveness of pancreatic β cells to Glibenclamide, subsequently could prevent the augmentation of insulin release induced by the drug. This finding is worthy to consider in metabolic control of diabetic patients whom consume the agent.
