Abstract
The pancreatic islet is a multicellular network comprised of a majority of excitable insulin-producing β-cells. Electrically active β-cells show oscillations in intracellular Ca2+ that lead to insulin release. β-cell electrical activity is coordinated by gap junction channels. β-cell Ca2+ activity is globally elevated at high glucose, whereas it is globally silenced at low glucose due to gap junction communication. Using multicellular computational models of mouse and human islet electrophysiology, we investigated the role highly functional β-cell subpopulations may play in driving islet Ca2+ dynamics.
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