Two-dimensional interaction of Ca²⁺ and IP₃ regulating insulin secretion in a pancreatic β-cell

The cellular storage and release of calcium ions (Ca 2+ ) are vital for a cell's survival. Within β-cells, these ions interact with various messengers to facilitate cellular signaling. One key messenger is inositol trisphosphate (IP 3 ), which regulates β-cell functions by interacting with Ca 2+ . This study presents a two-dimensional spatiotemporal mathematical model illustrating the interplay between Ca 2+ and IP 3 within a β-cell. The model is formulated as a system of reaction-diffusion equations, incorporating initial and boundary conditions based on β-cell physiology. For obtaining the numerical solution the finite element method with the Crank-Nicolson scheme has been used. Our results offer insights into the interdependent spatial and temporal influences of Ca 2+ and IP 3 dynamics, also their roles in insulin secretion. We analyze the effects of various channels and pumps, such as voltage-gated calcium channels (VGCC), plasma membrane calcium ATPases (PMCA), endoplasmic reticulum (ER) calcium leak, inositol trisphosphate receptors (IP 3 R), and sarco/endoplasmic reticulum calcium ATPases (SERCA), using the model. Furthermore, our findings shed light on the conditions linked to the development of Type-1 diabetes, Type-2 diabetes, and persistent hyperinsulinemic hypoglycemia of infancy (PHHI). We define the pathogenesis of these diseases as a novel disorder of the ER mechanism.