Nox2 contributes to hyperinsulinemia-induced redox imbalance and impaired vascular function.
Ontology highlight
ABSTRACT: Insulin resistance promotes vascular endothelial dysfunction and subsequent development of cardiovascular disease. Previously we found that skeletal muscle arteriolar flow-induced dilation (FID) was reduced following a hyperinsulinemic clamp in healthy adults. Therefore, we hypothesized that hyperinsulinemia, a hallmark of insulin resistance, contributes to microvascular endothelial cell dysfunction via inducing oxidative stress that is mediated by NADPH oxidase (Nox) system. We examined the effect of insulin, at levels that are comparable with human hyperinsulinemia on 1) FID of isolated arterioles from human skeletal muscle tissue in the presence and absence of Nox inhibitors and 2) human adipose microvascular endothelial cell (HAMECs) expression of nitric oxide (NO), endothelial NO synt
SUBMITTER: Mahmoud AM
PROVIDER: S-EPMC5466665 | biostudies-literature | 2017 Oct
REPOSITORIES: biostudies-literature
ACCESS DATA