The broad context of my ongoing research has been focused on understanding the physiological and pathological roles of ATP-sensitive potassium (KATP) channels. KATP channels are expressed in many tissues (brain, heart, muscle and pancreas) linking metabolism to membrane electrical activity. Mutations on ATP-sensitive K+ (KATP) channels are the main cause of several human diseases including Neonatal Diabetes Mellitus, Congenital Hyperinsulinism, brain disorders and Cantu syndrome. In pancreatic β--cells, KATP channels critically link glucose metabolism to insulin secretion. In the last few years, I focused my research on the role and consequences of altered KATP channels in insulin secretion; and more recently, on understanding the underlying mechanism/s of pancreatic β-cell exhaustion and glucotoxicity in diabetes . I have been also studying the consequences of altered KATP channels in extra-pancreatic tissues (heart, vasculature).

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