Glucose-stimulated insulin release from pancreatic islet β-cells involves increased levels of
reactive oxygen and nitrogen species. Although this is normal, under pathophysiological
conditions such as chronic hyperglycemia and inflammation, insulin exocytosis fails, and yet
the mechanistic reason for failure is unclear. Hypothesizing that exocytotic proteins might be
targets of S-nitrosylation, with their dysfunction under conditions of nitrosative stress serving
as a mechanistic basis for insulin secretory dysfunction, we identified the t-SNARE protein …