ArticleBulletin of mathematical biology1995
Correlations of rates of insulin release from islets and plateau fractions for beta-cells.
Article in Bulletin of mathematical biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Small subpopulations of β-cells do not drive islet oscillatory [Ca2+] dynamics via gap junction communication.PLoS computational biology · 2021Article
- Temporal plasticity of insulin and incretin secretion and insulin sensitivity following sleeve gastrectomy contribute to sustained improvements in glucose control.Molecular metabolism · 2019Article
- Obesity-dependent CDK1 signaling stimulates mitochondrial respiration at complex I in pancreatic β-cells.The Journal of biological chemistry · 2019Article
- Article
- Phase transitions in pancreatic islet cellular networks and implications for type-1 diabetes.Physical review. E, Statistical, nonlinear, and soft matter physics · 2014Article
Corrections and comments
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Authors and funding
2 authors.
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Abstract
Pancreatic beta-cells in intact islets of Langerhans perfused with various glucose concentrations exhibit periodic bursting electrical activity (BEA) consisting of active and silent phases. The fraction of the time spent in the active phase is called the plateau fraction and appears to be strongly correlated with the rate of release of insulin from islets as glucose concentration is varied. Here this correlation is quantified and a theoretical development is presented in detail. Experimental rates of insulin release are correlated with "effective" plateau fractions over a range of glucose concentrations. There are a number of different models for BEA in pancreatic beta-cells and a method is developed here to quantify the dependence of a glucose dependent parameter on glucose concentration. As an example, the plateau fractions computed from the Sherman-Rinzel-Keizer model are matched with experimental plateau fractions to obtain a relationship between the model's glucose-dependent parameter, beta, and glucose concentration. Knowledge of the relationships between beta and glucose concentration and between experimental measurements of rates of insulin release and plateau fractions permits the determination of theoretical rates of insulin release from the model.
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