Interestingly, several studies have shown that the disruption of sEH enhanced islet glucose-stimulated insulin secretion through AMPK signaling and decreased islet cell apoptosis in diabetes.447 Inhibiting sEH activity provided significant protection against islet β cell damage and improved glucose homeostasis in streptozotocin-induced diabetes.447,448 Moreover, 5,6-EET directly stimulates the release of insulin but has no effect on glucagon release. Here, PRKAA2 is linked to diabetes mellitus.