Showing 2 results for Pancreatic Islets
Mahmood Khayatian, Bagher Larijani, Bijan Farzami, Shirin Pournourmohammadi, Hoda Boushehri,
Volume 6, Issue 1 (8-2006)
Abstract
Background: Sulfonylurea agents such as Glibenclamide (Glyburide) have been widely prescribe in treatment of type 2 diabetic patients for decades, but controversy remains about their precise mechanism of action. On the other hand, glucokinase serves as a glucose sensor in pancreatic β-cells and plays a key role in the regulation of insulin secretion and glucose homeostasis. The aim of the present study was to evaluate the effect of Glibenclamide on insulin secretion and glucokinase activity in the rat isolated pancreatic islets of Langerhans.
Methods: The islets from normal and type 2 diabetic rats were isolated by collagenase digestion method. Glucokinase activity was measured via determination the rate of glucose-6-phosphate formation in the fluorometric assay. Insulin secretion from hand-picked islets was evaluated by static incubation technique. Insulin concentration was measured by rat insulin ELISA kit.
Results: Our findings obtained from incubation of Glybenclamide with pancreatic islets revealed that this agent increases basal insulin secretion (at 2.8 mM glucose) in both normal and diabetic rats as compared it with control islet (without drug). However, the increase of insulin secretion in response to 16.7 mM glucose was not significant. On the other hand, Glybenclamide had no activating and/or inhibiting effect on pancreatic glucokinase activity in both diabetic and normal Rats. But reduced activity of this enzyme in diabetic rats was significant in comparison with normal.
Conclusion: These data show that increasing effect of Glybenclamide on insulin secretion is through a mechanism other than affecting Glucose Mediated Insulin Release. Moreover, the regulation of pancreatic glucokinase does not depend on glybenclamid.
Mahsa Mohammad Amoli, Rohollah Mousavizadeh, Parvin Amiri, Bagher Larijani,
Volume 6, Issue 2 (9-2006)
Abstract
Background: Pancreatic islet transplantation has been reported as an appropriate method for treatment of type I diabetes patients, however there are strong indications that cytokine and chemokines secreted from transplanted islets play an important role in islet graft rejection in different stage post-transplantation. The NF-kB signaling pathway is activated in response to the stress resulted from isolation and purification process of pancreatic islets. Secretion and release of inflammatory mediators, including MCP-1, result from activation of this pathway which plays important part in activation of inflammatory processes accelerating graft rejection.
Methods: This study was performed to examine the effect of curcumin on secretion of inflammatory mediators and function of pancreatic islets.
Results: We observed that curcumin significantly decreased MCP-1 release from mouse islets compared to the control group and had no effect on function of pancreatic islets.
Conclusion: Investigating the stimulatory signals leading to production and secretion of inflammatory mediators from pancreatic islets and discovering their underlying mechanisms will be useful in finding new therapeutic interventions for blocking inflammatory pathways and improvement in outcome of islet cell transplantation.
