Protein kinase C-β contributes to impaired endothelial insulin signaling in humans with diabetes mellitus.

ABSTRACT:

Background

Abnormal endothelial function promotes atherosclerotic vascular disease in diabetes. Experimental studies indicate that disruption of endothelial insulin signaling, through the activity of protein kinase C-β (PKCβ) and nuclear factor κB, reduces nitric oxide availability. We sought to establish whether similar mechanisms operate in the endothelium in human diabetes mellitus.

Methods and results

We measured protein expression and insulin response in freshly isolated endothelial cells from patients with type 2 diabetes mellitus (n=40) and nondiabetic controls (n=36). Unexpectedly, we observed 1.7-fold higher basal endothelial nitric oxide synthase (eNOS) phosphorylation at serine 1177 in patients with diabetes mellitus (P=0.007) without a difference in total eNOS ex

SUBMITTER: Tabit CE 

PROVIDER: S-EPMC3572725 | biostudies-literature | 2013 Jan

REPOSITORIES: biostudies-literature