Endothelial nitric oxide synthase (eNOS) is activated by phosphorylation of serine 1177 by
the protein kinase Akt/PKB. Since hyperglycemia-induced mitochondrial superoxide …

There is some evidence that the endothelium dependent vasodilatation of coronary arteries
is impaired in both types of diabetes. The underlying mechanisms are not yet clear, in …

Background—Hyperglycemia impairs functional properties of cytosolic and nuclear proteins
via O-linked glycosylation modification (O-GlcNAcylation). We studied the effects of O …

Background—The vasodilatory effect of insulin can be acute or increase with time from 1 to 7
hours, suggesting that insulin may enhance the expression of endothelial nitric oxide …

Background Hyperglycemia is a primary cause of premature vascular disease. Endothelial
cell dysfunction characterized by diminished endothelium-dependent relaxations is likely to …

Recent studies have indicated that insulin activates endothelial nitric-oxide synthase (eNOS)
by protein kinase B (PKB)-mediated phosphorylation at Ser 1177 in endothelial cells …

Background Insulin sensitivity varies up to threefold in apparently healthy individuals, but the
mechanism for this is unknown. We have examined the hypothesis that vascular endothelial …

Diabetes is associated with endothelial dysfunction and increased risk of hypertension,
cardiovascular disease, and renal complications. Earlier studies have revealed that …

In the vasculature, nitric oxide (NO) is generated by endothelial NO synthase (eNOS) in a
calcium/calmodulin-dependent reaction. With oxidative stress, the critical cofactor BH 4 is …

Aims/hypothesis Hyperglycaemia is a primary cause of vascular complications in diabetes. A
hallmark of these vascular complications is endothelial cell dysfunction, which is partly due …