Mathematical models for insulin secretion in pancreatic β-cells.
ABSTRACT Insulin secretion is one of the most characteristic features of β-cell physiology. As it plays a central role in glucose regulation, a number of experimental and theoretical studies have been performed since the discovery of the pancreatic β-cell. This review article aims to give an overview of the mathematical approaches to insulin secretion. Beginning with the bursting electrical activity in pancreatic β-cells, we describe effects of the gap-junction coupling between β-cells on the dynamics of insulin secretion. Then, implications of paracrine interactions among such islet cells as α-, β-, and δ-cells are discussed. Finally, we present mathematical models which incorporate effects of glycolysis and mitochondrial glucose metabolism on the control of insulin secretion.
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ABSTRACT: Diabetes is a chronic and complex multifactorial disease caused by persistent hyperglycemia and for which underlying pathogenesis is still not completely understood. The mathematical modeling of glucose homeostasis, diabetic condition, and its associated complications is rapidly growing and provides new insights into the underlying mechanisms involved. Here, we discuss contributions to the diabetes modeling field over the past five decades, highlighting the areas where more focused research is required.CPT: Pharmacometrics & Systems Pharmacology (2013) 2, e54; doi:10.1038/psp.2013.30; advance online publication 10 July 2013.07/2013; 2:e54. DOI:10.1038/psp.2013.30
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ABSTRACT: A theoretical approach to the glucose–insulin regulatory system is presented. By means of integrated mathematical modeling and extensive numerical simulations, we probe the cell-level dynamics of the membrane potential, intracellular Ca2+ concentration, and insulin secretion in pancreatic β-cells, together with the whole-body level glucose–insulin dynamics in the liver, brain, muscle, and adipose tissues. In particular, the three oscillatory modes of insulin secretion are reproduced successfully. Such comprehensive mathematical modeling may provide a theoretical basis for the simultaneous assessment of the β-cell function and insulin resistance in clinical examination.Physics Letters A 10/2012; 376(45):3150–3157. DOI:10.1016/j.physleta.2012.08.006 · 1.63 Impact Factor