Key result
Stochastic perturbations in GLUT4 transport drive persistent temporal fluctuations in simulated diabetic myocardium.
Why the study?
A previous glucose-insulin interaction model incorporated a transportation delay associated with GLUT4-mediated glucose uptake, despite prior evidence indicating that GLUT4 recruitment exhibits stochastic behavior. This study therefore extends the model by introducing stochastic perturbations to examine the coupled dynamics of glucose transport and myocardial contractile function under diabetic conditions.
In-silico modeling demonstrates that stochasticity in GLUT4-mediated glucose transport causes persistent molecular fluctuations and constrains parameter recalibration in diabetic cardiac contractility.
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No immediate clinical implications for diabetic cardiomyopathy; leaves open whether stochastic GLUT4 effects translate beyond in-silico models.
The present in-silico study incorporates a stochastic framework for GLUT4 recruitment to examine the coupled dynamics of glucose transport and myocardial contractile function. In their previous study, Das et al. (2020) developed a glucose–insulin interaction model incorporating a transportation delay associated with GLUT4-mediated glucose uptake. However, prior evidence suggests that GLUT4 recruitment exhibits stochastic behavior. Accordingly, the present study extends the model by introducing stochastic perturbations into GLUT4-mediated glucose transport. The results indicate that stochasticity constrains parameter recalibration under diabetic conditions. Moreover, in the absence of delay, although the deterministic system attains a steady state, the stochastic counterpart exhibits persistent temporal fluctuations, inducing transient dynamics at the molecular level.
Das et al. (2026) studied Diabetes and cardiac contractility. Stochastic framework for GLUT4 recruitment vs. Deterministic glucose-insulin interaction model was evaluated on Coupled dynamics of glucose transport and myocardial contractile function. Stochastic perturbations in GLUT4-mediated glucose transport constrained parameter recalibration in diabetes and induced persistent temporal fluctuations in this in-silico model.