标签：
ADP, adenosine diphosphate ATP, adenosine triphosphate CK, Chay-Keizer CRAC, calcium release-activated current Ca2+, calcium ions DOM, dual oscillator model ER, endoplasmic reticulum F6P, fructose-6-phosphate FBP, fructose-1,6-bisphosphate GLUT, glucose transporter GSIS, glucose-stimulated insulin secretion HERG, human eter à-go-go related gene IP3R, inositol-1,4,5-trisphosphate receptors KATP, ATP-sensitive K+ channels KCa, Ca2+-dependent K+ channels Kv, voltage-dependent K+ channels MCU, mitochondrial Ca2+ uniporter NCX, Na+/Ca2+ exchanger PFK, phosphofructokinase PMCA, plasma membrane Ca2+-ATPase ROS, reactive oxygen species RyR, ryanodine receptors SERCA, sarco-endoplasmic reticulum Ca2+-ATPase T2D, Type 2 Diabetes TCA, trycarboxylic acid cycle TRP, transient receptor potential VDCC, voltage-dependent Ca2+ channels Vm, membrane potential [ATP]i, cytosolic ATP [Ca2+]i, intracellular calcium concentration [Ca2+]m, mitochondrial calcium [Na+], Na+ concentration action potentials bursting cAMP, cyclic AMP calcium electrical activity ion channels mNCX, mitochondrial Na+/Ca2+ exchanger mathematical model β-cell
Mathematical modeling of the electrical activity of the pancreatic β-cell has been extremely important for understanding the cellular mechanisms involved in glucose-stimulated insulin secretion. Several models have been proposed over the last 30 y, growing in complexity as experimental evidence of the cellular mechanisms involved has become available. Almost all the models have been developed based on experimental data from rodents. However, given the many important differences between species, models of human β-cells have recently been developed. This review summarizes how modeling of β-cells has evolved, highlighting the proposed physiological mechanisms underlying β-cell electrical activity.
