Dynamics of Computational Islet Simulations

Islets with majority mutated open K_ATP channels retain bursting

  • Gemma Gearhart Division of Science, Mathematics and Computing, Bard College at Simon’s Rock
  • Shuai Jiang
  • Thomas J. May
  • Jane Pan
  • Samuel Khuvis
  • Matthias K. Gobbert
  • Bradford E. Peercy
  • Arthur Sherman
Keywords: beta cell model, computational islet, glycolytic oscillations


The study of pancreatic beta-cells comprises a crucial part of the study of the group of diseases known as diabetes. These cells exist in groups known as islets of Langerhans and are responsible for storing and producing insulin. They exhibit electrical bursting behavior during insulin production that correlates with the rate at which insulin is secreted into the bloodstream. Coupling is a natural process within islets that enables the cells to communicate with one another and transfer various ions and electrical currents; coupling of both voltage and metabolites can occur. We model multicellular islets using an existing system of seven ordinary differential equations to model beta cell function. We simulate cells with mutated KATP channels that remain open indefinitely, which have been described in experimental studies but not yet modeled. Simulations ran with these mutations reveal the existence of a bursting death threshold, described by the least percentage of cells in the islet that must be mutated for electrical bursts to completely disappear. We determine that this threshold is independent of coupling strengths, cell distribution, and possibly islet dimension; however, we also determined that this threshold is dependent on the glucose influx rate.

How to Cite
Gearhart, Gemma, Shuai Jiang, Thomas J. May, Jane Pan, Samuel Khuvis, Matthias K. Gobbert, Bradford E. Peercy, and Arthur Sherman. 2014. “Dynamics of Computational Islet Simulations”. Letters in Biomathematics 1 (1), 3-15. https://doi.org/10.1080/23737867.2014.11414466.