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Vehpi Yildirim


Speaker: Vehpi Yildirim
Title: A Mathematical Model for Bursting Electrical Activity Recovery in Pancreatic Beta Cells
Affiliation: Florida State University
Date: Wednesday, December 3, 2014
Place and Time: Room 200, Love Building, 3:35 pm

Abstract. Insulin is the bodies only hormone capable of reducing blood glucose level and secreted from pancreatic beta cells. Secretion is oscillatory, which is resulted from bursting electrical activity of the cell. Secretion process is initiated by glucose uptake. Inside the cell glucose is metabolized and ATP is produced in expense for ADP. Increased ATP concentration blocks ATP sensitive potassium channels (K(ATP) channels) and depolarize the cell. Depolarization increases Ca(2+) influx, which leads exocytosis of filled granules and insulin secretion. In the process K(ATP) channels play a significant role by coupling cell metabolism to membrane potential. A mutation in the genes encoding K(ATP) channel proteins causes spontaneous depolarization of the cell and the loss of bursting electrical activity, which results with persistent hyperinsulinemic hypoglycemia of infancy (PHHI) in humans. PHHI is a pathological condition characterized with high insulin secretion despitlow blood glucose. However SUR1(-/-) mice beta-cells, lacking functional K(ATP) channels, exhibit bursting electrical activity and almost normal blood glucose levels. In these mice an alternative mechanism must be compensating for the lack of K(ATP) channels. One hypothesis suggests that, this compensation might be resulted from up regulation of an alternative ion channel, which is based on the idea that long term changes in the cell activity regulates \gene expression in many excitable cells. We introduce and analyze and activity dependent recovery mechanism for genetically engineered mice beta cells, via which model cell keeps track of the activity and regulates expression of an alternative channel to restore a target activity.