Version 1
: Received: 23 April 2024 / Approved: 23 April 2024 / Online: 23 April 2024 (13:48:31 CEST)
How to cite:
MAHAPATRA, C.; Shanmugam, K. Computational Modeling of Sodium Ion Channel-Based Glucose Sensing Biophysics to Study Abnormal Electrical Activities in Cardiac Atrial Cell. Preprints2024, 2024041524. https://doi.org/10.20944/preprints202404.1524.v1
MAHAPATRA, C.; Shanmugam, K. Computational Modeling of Sodium Ion Channel-Based Glucose Sensing Biophysics to Study Abnormal Electrical Activities in Cardiac Atrial Cell. Preprints 2024, 2024041524. https://doi.org/10.20944/preprints202404.1524.v1
MAHAPATRA, C.; Shanmugam, K. Computational Modeling of Sodium Ion Channel-Based Glucose Sensing Biophysics to Study Abnormal Electrical Activities in Cardiac Atrial Cell. Preprints2024, 2024041524. https://doi.org/10.20944/preprints202404.1524.v1
APA Style
MAHAPATRA, C., & Shanmugam, K. (2024). Computational Modeling of Sodium Ion Channel-Based Glucose Sensing Biophysics to Study Abnormal Electrical Activities in Cardiac Atrial Cell. Preprints. https://doi.org/10.20944/preprints202404.1524.v1
Chicago/Turabian Style
MAHAPATRA, C. and Kirubanandan Shanmugam. 2024 "Computational Modeling of Sodium Ion Channel-Based Glucose Sensing Biophysics to Study Abnormal Electrical Activities in Cardiac Atrial Cell" Preprints. https://doi.org/10.20944/preprints202404.1524.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.
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.
