Does GLUT4 Queue? A Mechanistic Mathematical Model for Insulin Response in Adipocytes

Mammalian cells regulate their glucose levels by redistributing glucose transporter proteins within the cell. Glucose Transporter 4 (GLUT4) is the main insulin-regulated glucose transporter in mammalian cells. Insulin signals the redistribution of GLUT4 from intracellular compartments to the cell surface. The mechanisms of the release of GLUT4 and subsequent transport to the plasma membrane remain an open question. Here, a biologically plausible model of GLUT4 translocation is presented. Using a stochastic queuing model, we find that changing only the number of fusion sites available for GLUT4-containing vesicles as a function of insulin is sufficient to explain experimental observations. Thus, the activity of the fusion sites could be the primary determinant of the dynamics of GLUT4.

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Publication Details

Journal
Bulletin of Mathematical Biology
Published
2025-09-02
DOI
https://doi.org/10.1007/s11538-025-01490-6
Primary Topic
Metabolism, Diabetes, and Cancer
Type
article
Field-Weighted Citation Impact
0.00

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article

Does GLUT4 Queue? A Mechanistic Mathematical Model for Insulin Response in Adipocytes

Brock D. Sherlock, Maria Vlasiou, Marko Boon, Adelle C.F. Coster
Bulletin of Mathematical Biology
Metabolism, Diabetes, and Cancer
article

Does GLUT4 Queue? A Mechanistic Mathematical Model for Insulin Response in Adipocytes

Brock D. Sherlock, Maria Vlasiou, Marko Boon, Adelle C.F. Coster
article en

Abstract

Mammalian cells regulate their glucose levels by redistributing glucose transporter proteins within the cell. Glucose Transporter 4 (GLUT4) is the main insulin-regulated glucose transporter in mammalian cells. Insulin signals the redistribution of GLUT4 from intracellular compartments to the cell surface. The mechanisms of the release of GLUT4 and subsequent transport to the plasma membrane remain an open question. Here, a biologically plausible model of GLUT4 translocation is presented. Using a stochastic queuing model, we find that changing only the number of fusion sites available for GLUT4-containing vesicles as a function of insulin is sufficient to explain experimental observations. Thus, the activity of the fusion sites could be the primary determinant of the dynamics of GLUT4.

Bulletin of Mathematical BiologyVol. 87(10)
UNSW Sydney (AU), Eindhoven University of Technology (NL), University of Twente (NL)
Australian Government, Australian Research Council
Openalex Percentile: Top 80%
Metabolism, Diabetes, and Cancer
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