Objectives: The development of microvascular complications in diabetes is a complex
process in which endothelial dysfunction is important. Emerging evidence suggests that
arginase is a key mediator of endothelial dysfunction in type 2 diabetes mellitus by
reciprocally regulating nitric oxide bioavailability. The aim of this prospective intervention
study was to test the hypothesis that arginase activity is increased and that arginase
inhibition improves microvascular endothelial function in patients with type 2 diabetes and …

Background Arginase is implicated in the pathogenesis behind endothelial dysfunction in
type 2 diabetes mellitus (T2 DM) by its inhibition of nitric oxide formation. Strict glycaemic
control is not sufficient to improve endothelial function or cardiovascular outcomes in
patients with T2 DM, thus other treatment strategies are needed. We hypothesized that
arginase inhibition improves endothelial function beyond glucose‐lowering therapy
following glucose optimization in patients with poorly controlled T2 DM. Methods and results …