A UCP2 activity inmammalian β-pancreatic cells has been implicated in the development ofType II diabetes by altering the ATP/ADP ratio, causing the KATPchannel to stay open and leading to decreased insulinsecretion [4, 5, 9, 31].To further strengthen our transgenic system as a genetic model for diabetes, wehave taken electrophysiological approaches to understand the mechanism wherebyincreased UCP activity modulates the release of DILPs in Drosophilaadult IPCs. The gene discussed is UCP2; the disease is diabetes mellitus.