Disturbances in system dynamics of C a 2 + and I P 3 perturbing insulin secretion in a pancreatic β -cell due to type-2 diabetes.

The individual study of $C{a}^{2+}$ and $I{P}_3$ dynamics respectively in a $\beta$-cell has yielded limited information about the cell functions. But the systems biology approaches for such studies have received very little attention by the research workers in the past. In the present work, a system-dynamics model for the interdependent $C{a}^{2+}$ and $I{P}_3$ signaling that controls insulin secretion in a $\beta$-cell has been suggested. A two-way feedback system of $C{a}^{2+}$ and $I{P}_3$ has been considered and one-way feedback between $C{a}^{2+}$ and insulin has been implemented in the model. The finite element method along with the Crank-Nicolson method have been applied for simulation. Numerical results have been used to analyze the impact of perturbations in $C{a}^{2+}$ and $I{P}_3$ dynamics on insulin secretion for normal and Type-2 diabetic conditions. The results reveal that Type-2 diabetes comes from abnormalities in insulin secretion caused by the perturbation in buffers and pumps (SERCA and PMCA).