Numerical simulation of calcium dynamics dependent ATP degradation, IP3 and NADH production due to obesity in a hepatocyte cell

Calcium (Ca2+) signals have a crucial role in regulating various processes of almost every cell to maintain its structure and function. Calcium dynamics has been studied in various cells including hepatocytes by many researchers, but the mechanisms of calcium signals involved in regulation and dysregulation of various processes like ATP degradation rate, IP3 and NADH production rate respectively in normal and obese cells are still poorly understood. In this paper, a reaction diffusion equation of calcium is employed to propose a model of calcium dynamics by coupling ATP degradation rate, IP3 and NADH production rate in hepatocyte cells under normal and obese conditions. The processes like source influx, buffer, endoplasmic reticulum (ER), mitochondrial calcium uniporters (MCU) and Na+/Ca2+ exchanger (NCX) have been incorporated in the model. Linear finite element method is used along spatial dimension, and Crank-Nicolson method is used along temporal dimension for numerical simulation. The results have been obtained for the normal hepatocyte cells and for cells due to obesity. The comparative study of these results reveal significant difference caused due to obesity in Ca2+ dynamics as well as in ATP degradation rate, IP3 and NADH production rate.

Automated summary

In this study, a model of calcium dynamics is proposed by using a reaction diffusion equation to investigate the mechanisms of calcium signals in regulating ATP degradation rate, IP3 and NADH production rate in normal and obese cells. The model incorporates processes like source influx, buffer, endoplasmic reticulum, mitochondrial calcium uniporters, and Na+/Ca2+ exchanger. The results show significant differences in Ca2+ dynamics as well as in ATP degradation rate, IP3 and NADH production rate caused by obesity.