Simulation of the autonomic neural control of insulin secretion

Abstract

A seventh order, nonlinear, highly isomorphic, dynamic systems model of insulin secretion was used to test specific mechanistic hypotheses about the sites of action of sympathetic and parasympathetic autonomic neural input on glucose-induced insulin secretion. The application of neural input was modeled by changing only those specific model parameters that correspond to the hypotheses under study as a function of the input magnitude. The results of these simulations suggest that sympathetic and parasympathetic inputs modify glucose-induced insulin secretion by decreasing the maximal rate of calcium uptake and increasing the affinity of calcium uptake to glucose, respectively.