Figure 1. Models of insulin secretion.

According to current models of insulin release, rapid mobilization of docked and primed granules (green arrow, A), elicits the 1st phase of insulin secretion (B). Although elevated glucose is the physiological stimulus, plasma membrane depolarization and changes in Ca²⁺ concentrations can be enough to stimulate hormone output at this point. Continued glucose metabolism (C), essential for sustained recruitment of granules (red arrows, A) contributes to prolonged, 2nd phase of insulin release (red arrow, B, D). ‘Incretins’ (for example, GIP, GLP-1, FFAs), as ligands for G protein coupled receptors (GPCRs) can further amplify the secretory response. The details of how infection impacts the full spectrum of GPCR-related signaling pathways are incompletely understood, but available evidence suggests that T cruzi parasite attenuates glucose and FFA stimulated insulin secretion and impairs the mobilization of the docked granule pool (D).