Since surprisingly even short-time (∼60 min) exposure of islets to high glucose in healthy animals was associated with enhanced production of iNOS-derived NO [7], [11], the present investigation was undertaken to study islet NOS activities and the influence of GLP-1 on an animal model of spontaneous type 2 diabetes and “glucotoxicity”, the mildly diabetic Goto-Kakizaki (GK) rat, which is considered a good model of human type 2 nonobese diabetes [15], [16], [17], [18]. The gene discussed is NOS1; the disease is type 2 diabetes mellitus.