COEXISTENCE OF THREE OSCILLATORY MODES OF INSULIN SECRETION: MATHEMATICAL MODELING AND RELEVANCE TO GLUCOSE REGULATION

DOI10.1142/S0218339017500188MaRDI QIDQ5348797zbMATH OpenOpenAlexWikidataFDO

Authors Hyuk Kang, Kyungreem Han, Segun Goh, M. Y. Choi

Publication date 21 August 2017

Published in Journal of Biological Systems (Search for Journal in Brave)

Full work available at URL https://doi.org/10.1142/s0218339017500188

zbMATH Keywords

simulationsmodelingdiabetespancreatic \(\beta\)-cellsoscillatory insulin secretionwhole-body glucose regulation

Mathematics Subject Classification ID

Biochemistry, molecular biology (92C40) Systems biology, networks (92C42)

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Cites work

• A simplified model for mitochondrial ATP production
• An islet population model of the endocrine pancreas
• Modeling the glucose-insulin regulatory system and ultradian insulin secretory oscillations with two explicit time delays

Cited in

(15)

• Hormonal effects on glucose regulation
• Delay in ATP-dependent calcium inflow may affect insulin secretion from pancreatic beta-cell
• Selective regulation of the insulin-Akt pathway by simultaneous processing of blood insulin pattern in the liver
• Diffusion induced oscillatory insulin secretion
• Modelling of energy-driven switch for glucagon and insulin secretion
• Beneficial effects of intercellular interactions between pancreatic islet cells in blood glucose regulation
• A model for ultradian oscillations of insulin and glucose
• Sustained simultaneous glycolytic and insulin oscillations in \(\beta\)-cells
• Mathematical modeling of insulin secretion and the role of glucose-dependent mobilization, docking, priming and fusion of insulin granules
• Dynamical modeling the effect of glucagon-like peptide on glucose-insulin regulatory system based on mice experimental observation
• Modelling the effect of CSII on the control of glucose concentration in type 1 diabetes
• Integrated multiscale mathematical modeling of insulin secretion reveals the role of islet network integrity for proper oscillatory glucose-dose response
• Heterogeneous alpha-cell population modeling of glucose-induced inhibition of electrical activity
• A novel model and its analysis on the metabolic regulations of glucose, insulin, and glucagon
• Lessons from models of pancreatic \(\beta \) cells for engineering glucose-sensing cells

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