Glucose response to bursting-spiking pancreatic ?-cells by a barrier kinetic model
- 1 September 1985
- journal article
- research article
- Published by Springer Nature in Biological Cybernetics
- Vol. 52 (5) , 339-349
- https://doi.org/10.1007/bf00355756
Abstract
A mathematical model of the pancreatic β-cell electrical activity was developed using a barrier kinetic model. Our model incorpolates the glucose sensitive channel which is known to conduct K+ in the absence of glucose. The model also incorporates Ca i sensitive K+ channels which are inhibited by intracellular H+ ions. It is described by three non-linear simultaneous differential equations. Numerical integration of these equations allowed us to examine the effect of glucose and of external Ca2+ ions on the electrical and cellular activity of the β-cell. Our results show that the contribution of glucose-sensitive channel activity, if not completely inhibited, plays a very important role in determining the bursting periodicity. Our results also shows that even a small decrease in pH i is sufficient to change a bursting β-cell to a spiking one. The voltage dependence of calcium sensitive K+ channels, however, affects little to the bursting mode of the electrical activity. Our simulation supports an incomplete selectivity of the voltage dependent calcium channel for calcium ions with low external [Ca2+]. It also supports the role of [Ca] i as an inhibitor of this channel when [Ca] i becomes unusually high.This publication has 42 references indexed in Scilit:
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