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• W2021025717 abstract "Background— Inflammatory mechanisms could be involved in the pathogenesis of both insulin resistance and atherosclerosis. Therefore, we aimed at examining whether the proinflammatory cytokine tumor necrosis factor (TNF)-α inhibits insulin-stimulated glucose uptake and insulin-stimulated endothelial function in humans. Methods and Results— Healthy, lean male volunteers were studied. On each study day, 3 acetylcholine (ACh) or sodium nitroprusside (SNP) dose-response studies were performed by infusion into the brachial artery. Before and during the last 2 dose-response studies, insulin and/or TNF-α were coinfused. During infusion of insulin alone for 20 minutes, forearm glucose uptake increased by 220±44%. This increase was completely inhibited during coinfusion of TNF-α (started 10 min before insulin) with a more pronounced inhibition of glucose extraction than of blood flow. Furthermore, TNF-α inhibited the ACh forearm blood flow response ( P <0.001), and this inhibition was larger during insulin infusion ( P =0.01) but not further increased by N G -monomethyl- l -arginine acetate ( P =0.2). Insulin potentiated the SNP response less than the ACh response and the effect of TNF-α was smaller ( P <0.001); TNF-α had no effect on the SNP response without insulin infusion. Thus, TNF-α inhibition of the combined response to insulin and ACh was likely mediated through inhibition of NO production. Conclusion— These results support the concept that TNF-α could play a role in the development of insulin resistance in humans, both in muscle and in vascular tissue." @default.
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• W2021025717 date "2003-10-14" @default.
• W2021025717 modified "2023-10-14" @default.
• W2021025717 title "Tumor Necrosis Factor-α Inhibits Insulin’s Stimulating Effect on Glucose Uptake and Endothelium-Dependent Vasodilation in Humans" @default.
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• W2021025717 doi "https://doi.org/10.1161/01.cir.0000091406.72832.11" @default.
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