ArticleDiabetologia2009
Endothelial inflammation induced by excess glucose is associated with cytosolic glucose 6-phosphate but not increased mitochondrial respiration.
Article in Diabetologia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 50 citations in OpenAlex.
- Gene expression changes in adipose tissue with diet- and/or exercise-induced weight loss.Cancer prevention research (Philadelphia, Pa.) · 2013Trial
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- Rates of Mitochondrial Metabolism of Glucose, Amino Acids, and Fatty Acids by the HEI-OC1 Inner Ear Cell Line.Biology · 2025Article
- Serine supplementation suppresses hypoxia-induced pathological retinal angiogenesis.Theranostics · 2025Article
- Benefits of Cilostazol's Effect on Vascular and Neuropathic Complications Caused by Diabetes.Medical sciences (Basel, Switzerland) · 2024Review
- Hyperglycemic conditions induce rapid cell dysfunction-promoting transcriptional alterations in human aortic endothelial cells.Scientific reports · 2022Article
- Curcumin activates autophagy and attenuates high glucose-induced apoptosis in HUVECs through the ROS/NF-κB signaling pathway.Experimental and therapeutic medicine · 2022Article
- Cre toxicity in mouse models of cardiovascular physiology and disease.Nature cardiovascular research · 2022Article
- Oxidative Stress in Type 2 Diabetes: The Case for Future Pediatric Redoxomics Studies.Antioxidants (Basel, Switzerland) · 2022Review
- Brain Endothelial Cells Utilize Glycolysis for the Maintenance of the Transcellular Permeability.Molecular neurobiology · 2022Article
- High glucose enhances lipopolysaccharide-induced inflammation in cultured BV2 microglial cell line.Immunity, inflammation and disease · 2022Article
- Glucose consumption of vascular cell types in culture: toward optimization of experimental conditions.American journal of physiology. Cell physiology · 2022Article
- Fluidics system for resolving concentration-dependent effects of dissolved gases on tissue metabolism.eLife · 2021Article
- Inflammation in Metabolic Cardiomyopathy.Frontiers in cardiovascular medicine · 2021Review
- The effects of humic water on endothelial cells under hyperglycemic conditions: inflammation-associated parameters.Environmental geochemistry and health · 2019Article
- Mitochondrial regulation of diabetic vascular disease: an emerging opportunity.Translational research : the journal of laboratory and clinical medicine · 2018Review
- A method for high-throughput functional imaging of single cells within heterogeneous cell preparations.Scientific reports · 2016Article
- Low-level laser irradiation effect on endothelial cells under conditions of hyperglycemia.Lasers in medical science · 2016Article
- Blood-cell bioenergetics are associated with physical function and inflammation in overweight/obese older adults.Experimental gerontology · 2015Article
- TallyHO obese female mice experience poor reproductive outcomes and abnormal blastocyst metabolism that is reversed by metformin.Reproduction, fertility, and development · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
aims/hypothesisExposure 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.
methodsThe effects of glycolytic and mitochondrial fuels on metabolic intermediates and end-products of glycolytic and oxidative metabolism, including glucose 6-phosphate (G6P), lactate, CO(2), NAD(P)H and OCR, were measured in cultured human microvascular endothelial cells and correlated with IkappaBalpha phosphorylation.
resultsIn response to increases in glucose concentration from low to physiological levels (0-5 mmol/l), production of G6P, lactate, NAD(P)H and CO(2) each increased as expected, while OCR was sharply reduced. IkappaBalpha activation was detected at glucose concentrations >5 mmol/l, which was associated with parallel increases of G6P levels, whereas downstream metabolic pathways were insensitive to excess substrate. CONCLUSIONS/
interpretationPhosphorylation of IkappaBalpha by excess glucose correlates with increased levels of the glycolytic intermediate G6P, but not with lactate generation or OCR, which are inhibited well below saturation levels at physiological glucose concentrations. These findings suggest that oxidative stress due to increased mitochondrial respiration is unlikely to mediate endothelial inflammation induced by excess glucose and suggests instead the involvement of G6P accumulation in the adverse effects of hyperglycaemia on endothelial cells.
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