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Computational Reconstruction of Pancreatic Islets as a Tool for Structural and Functional Analysis
Published on: March 9, 2022
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Critical transitions in pancreatic islets.
D Korošak1,2, S Postić3, A Stožer1
1University of Maribor, Faculty of Medicine, Institute for Physiology, Maribor, Slovenia.
Arxiv
|November 6, 2024
Summary
Pancreatic beta cells exhibit a critical, first-order phase transition in calcium signaling, characterized by hysteresis, as glucose levels change. This finding reveals islets as tipping elements crucial for abrupt insulin release.
Area of Science:
- Cellular biology
- Biophysics
- Physiology
Background:
- Pancreatic beta cells regulate insulin secretion through collective calcium (Ca2+) signaling.
- The transition of Ca2+ signaling from uncorrelated to correlated states resembles a phase transition but its order is not well understood.
Purpose of the Study:
- To investigate the nature and order of the phase transition in collective calcium signaling within pancreatic beta cells.
- To understand the role of islets as tipping elements in pancreatic function and insulin release.
Main Methods:
- Utilized confocal microscopy to record collective Ca2+ activation in intact pancreatic islets.
- Applied varying glucose concentrations in both increasing and decreasing patterns.
- Developed a network model of beta cells incorporating link selection and coordination.
Main Results:
- Observed a sharp transition in Ca2+ signaling from uncorrelated to correlated states as glucose concentration changed.
- Demonstrated hysteresis in the coordinated Ca2+ response, indicating a first-order phase transition.
- The network model successfully replicated the observed hysteresis loop and critical transition dynamics.
Conclusions:
- Collective calcium signaling in pancreatic beta cells undergoes a critical, first-order phase transition.
- Islets function as tipping elements, with their interconnectedness driving abrupt insulin release dynamics.
- Understanding these transitions is key to comprehending pancreatic islet function in glucose homeostasis.
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