Showing 2 results for Khayatian
Mahmood Khayatian, Bijan Farzami, Ebrahim Mirzajani, Bagher Larijani, Mohammad Taghikhani, S. Zahra Bathaei, Safoora Vardasbi, Esmael Elmi-Akhouni,
Volume 5, Issue 2 (18 2005)
Abstract
Background: Glucokinase serves as a glucose sensor in pancreatic β-cells and plays a key role in glucose homeostasis and glucose-stimulated insulin secretion (GSIS). In the present study we examined the effect of glucosamine, a glucokinase inhibitor, on the pancreatic glucokinase and hexokinase activities and on insulin secretion from freshly rat pancreatic islets of Langerhans. Insulin concentration was measured by rat insulin ELISA kit.
Methods: The pancreatic islets from normal and type 2 diabetic (nSTZ) rats were isolated by collagenase digestion method. Glucose phosphorylation was quantitated by measuring the rate of glucose-6-phosphate formation in the fluorometric assay. Insulin secretion from hand-picked islets was evaluated in static incubation system. Insulin concentration was measured by rat insulin ELISA kit.
Results: Our findings demonstrate that glucosamine in a dose dependent manner, reduced glucokinase activity in islet extract, but had no effect on hexokinase activity. The glucose-stimulated insulin secretion, was inhibited by glucosamine but it had no effect on the basal insulin secretion. In diabetic rats glucokinase was decreased while the basal insulin secretion and the activity of hexokinase were higher than normals.
Conclusion: Based on results obtained from the present study, the assumption could be made that the decrease in the activity of glucokinase of pancreatic islets could be related to the impaired glucose stimulated insulin secretion. The increase in basal insulin secretion of diabetic rats may be due to an increase in pancreatic hexokinase activity.
Mahmood Khayatian, Bagher Larijani, Bijan Farzami, Shirin Pournourmohammadi, Hoda Boushehri,
Volume 6, Issue 1 (19 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.
