2D Model for Ca2+ Dynamics Regulating IP3,ATP and Insulin in A Pancreatic β-Cell

The regulation of insulin in pancreatic beta-cells is dependent on changes in thecytoplasmic calcium concentration ([Ca2+](i)). The well-balanced influx andefflux routes are required for insulin secretion. Therefore, this researchpresents a simplified yet valuable model for investigating calcium dynamics ina beta-cell under 2D unsteady state conditions. The model integrates diffusion,reactions involving sources, excess buffers, and fluxes, including effluxthrough leak and SERCA mechanisms. Boundary and initial conditions aretailored to beta-cell physiology. Numerical solutions are computed using thefinite element method with co-axial circular elements, chosen for theireffectiveness in discretizing the cell domain and improving accuracy. Thisapproach minimizes errors, enhancing predictive fidelity and capturing theintricate geometries and dynamics within beta-cells. The model's findingshighlight the influence of buffers and source influx on calcium regulation, andintegrate temporal fluctuations inIP3(Inositol 1,4,5-Trisphosphate) synthesisand degradation, Adenosine Triphosphate (ATP) generation, insulin release,and metabolic processes. Computational analysis suggests disruptions incellular energy production and metabolite distribution may underlieconditions like metabolic syndrome and diabetes. This study contributes to adeeper understanding of beta-cell biology, potentially informing therapeuticstrategies for related disorders.