|
BIOMATHEMATICS SEMINAR
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.
|
