Metformin ameliorates dysfunctional traits of glibenclamide- and glucose-induced insulin secretion by suppression of imposed overactivity of the islet nitric oxide synthase-no system
Metformin lowers diabetic blood glucose primarily by reducing hepatic gluconeogenesis and increasing peripheral glucose uptake. However, possible effects by metformin on beta-cell function are incompletely understood. We speculated that metformin might positively influence insulin secretion through impacting the beta-cell nitric oxide synthase (NOS)-NO system, a negative modulator of glucose-stimu