Abnormally decreased NO and augmented CO production in islets of the leptin-deficient ob/ob mouse might contribute to explain hyperinsulinemia and islet survival in leptin-resistant type 2 obese diabetes

► Our recent data showed that CO has a signaling messenger function in rodent pancreatic islets. ► Present results show that islets from young and adult ob/ob mice displayed very low NO production. ► In contrast, production of CO, a NOS inhibitor, was impressively raised in ob/ob mice. ► While GLP-1 and GIP suppressed NOS activities from ob/ob mice leptin had opposite effects. ► This beneficial effect might have its clinical counterpart in human type 2 obese diabetes.