Version 1
: Received: 26 April 2024 / Approved: 27 April 2024 / Online: 28 April 2024 (10:58:05 CEST)
How to cite:
Mahapatra, C.; Shanmugam, K. In Silico Exploration of Sodium Ion Channel-Mediated Glucose Sensing Biophysics to Study Cardiac Atrial Cells Electrophysiology. Preprints2024, 2024041797. https://doi.org/10.20944/preprints202404.1797.v1
Mahapatra, C.; Shanmugam, K. In Silico Exploration of Sodium Ion Channel-Mediated Glucose Sensing Biophysics to Study Cardiac Atrial Cells Electrophysiology. Preprints 2024, 2024041797. https://doi.org/10.20944/preprints202404.1797.v1
Mahapatra, C.; Shanmugam, K. In Silico Exploration of Sodium Ion Channel-Mediated Glucose Sensing Biophysics to Study Cardiac Atrial Cells Electrophysiology. Preprints2024, 2024041797. https://doi.org/10.20944/preprints202404.1797.v1
APA Style
Mahapatra, C., & Shanmugam, K. (2024). In Silico Exploration of Sodium Ion Channel-Mediated Glucose Sensing Biophysics to Study Cardiac Atrial Cells Electrophysiology. Preprints. https://doi.org/10.20944/preprints202404.1797.v1
Chicago/Turabian Style
Mahapatra, C. and Kirubanandan Shanmugam. 2024 "In Silico Exploration of Sodium Ion Channel-Mediated Glucose Sensing Biophysics to Study Cardiac Atrial Cells Electrophysiology" Preprints. https://doi.org/10.20944/preprints202404.1797.v1
Abstract
Elevated blood glucose levels, known as glycemia, play a significant role in sudden cardiac arrest, often resulting in sudden cardiac death, particularly among those with diabetes. Understanding this link has been a challenge for healthcare professionals, leading many research groups to investigate the relationship between blood glucose levels and cardiac electrical activity. Our hypothesis suggests that glucose-sensing mechanisms in cardiac tissue could clarify this connection. To explore this, we adapted a single-compartment, in-silico model of the human atrial node's action potential. We incorporated glucose-sensing mechanisms with voltage-gated sodium ion channels using ordinary differential equations. Parameters for the model were based on existing experimental studies to mimic the impact of glucose levels on atrial node action potential firing. Simulations using voltage clamp and current clamp techniques showed that elevated glucose levels decreased sodium ion channel currents, leading to a reduction in the sinoatrial node action potential frequency. In summary, our model provides a cellular-level understanding of how high glucose levels can lead to bradycardia and sudden cardiac death.
Keywords
glucose sensor; ion channel; heart failure; in silico approach, computational modeling; sinoatrial node; action potential
Subject
Biology and Life Sciences, Biophysics
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.