This is a 3rd party implementation of Fridlyand & Philipson 2016 who's abstract begins "Insulin secretory in pancreatic beta-cells responses to nutrient stimuli and hormonal modulators include multiple messengers and signaling pathways with complex interdependencies. Here we present a computational model that incorporates recent data on glucose metabolism, plasma membrane potential, G-protein-coupled-receptors (GPCR), cytoplasmic and endoplasmic reticulum calcium dynamics, cAMP and phospholipase C pathways that regulate interactions between second messengers in pancreatic beta-cells. The values of key model parameters were inferred from published experimental data. The model gives a reasonable fit to important aspects of experimentally measured metabolic and second messenger concentrations and provides a framework for analyzing the role of metabolic, hormones and neurotransmitters changes on insulin secretion. Our analysis of the dynamic data provides support for the hypothesis that activation of Ca2+-dependent adenylyl cyclases play a critical role in modulating the effects of glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and catecholamines. ..."

Model Type: Channel/Receptor; Neuron or other electrically excitable cell

Region(s) or Organism(s): Human

Currents: Ca pump; ATP-senstive potassium current

Receptors: Adrenergic; Muscarinic; IP3; M3; Cholinergic Receptors

Transmitters: Acetylcholine; Norephinephrine; Ephinephrine; Ions

Model Concept(s): Calcium dynamics; Electrical-chemical; G-protein coupled; Ion Channel Kinetics

Simulation Environment: MATLAB

Implementer(s): Althaf, Athil A Z ; Mishra, Urvi ; Konnur, Seeraja [seeraja.dsa at gmail.com]

References:

Fridlyand LE, Philipson LH. (2016). Pancreatic Beta Cell G-Protein Coupled Receptors and Second Messenger Interactions: A Systems Biology Computational Analysis. PloS one. 11 [PubMed]