01975nas a2200145   4500008004100000245012600041210006900167260000800236490000700244520137300251100002701624700002801651700002201679856012801701       2024                        eng d00aComputational modeling of sodium-ion-channel-based glucose sensing biophysics to study cardiac pacemaker action potential0 aComputational modeling of sodiumionchannelbased glucose sensing   cSEP0 v293 a<p>
	<span style="font-family: Arial, Arial, Helvetica, sans-serif; font-size: 13.2px; text-align: justify;">Elevated blood glucose levels, known as hyperglycemia, play a significant role in sudden cardiac arrest, often resulting in sudden cardiac death, particularly among those with diabetes. Understanding the internal mechanisms 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 biophysics mechanisms in cardiac tissue could clarify this connection. To explore this, we adapted a single-compartment computational model of the human pacemaker 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 pacemaker 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 pacemaker action potential frequency. In summary, our mathematical model provides a cellular-level understanding of how high glucose levels can lead to bradycardia and sudden cardiac death.</span></p>
1 aMahapatra, Chitaranjan1 aShanmugam, Kirubanandan1 aRusho, Maher, Ali  uhttps://library.ncl.res.in/content/computational-modeling-sodium-ion-channel-based-glucose-sensing-biophysics-study-cardiac