Based on the described interaction between islet endothelial cells and β‐cell function, it is conceivable that the blunted insulin secretory responsiveness to a glucose load and the impaired glucose tolerance observed in the eNOS+/− mice in the present study could be at least in part due to a defective generation of NO by the islet endothelial cells and consequent reduction of islet microcirculatory vasodilation. This evidence concerns the gene INS and Impaired glucose tolerance.