Endothelial inflammation induced by excess glucose is associated with cytosolic glucose 6-phosphate but not increased mitochondrial respiration.

Publication Type:

Journal Article


Diabetologia, Volume 52, Issue 5, p.921-31 (2009)


2009, Cells, Cultured, Clinical Research Division, Endothelium, Vascular, Glucose, Glucose-6-Phosphate, Humans, Hyperglycemia, INFLAMMATION, Interleukin-6, Kinetics, Microcirculation, mitochondria, Oxygen Consumption


Exposure of endothelial cells to high glucose levels suppresses responses to insulin, including induction of endothelial nitric oxide synthase activity, through pro-inflammatory signalling via the inhibitor of nuclear factor kappaB (IkappaB)alpha-nuclear factor kappaB (NF-kappaB) pathway. In the current study, we aimed to identify metabolic responses to glucose excess that mediate endothelial cell inflammation and insulin resistance. Since endothelial cells decrease their oxygen consumption rate (OCR) in response to glucose, we hypothesised that increased mitochondrial function would not mediate these cells' response to excess substrate.