[HTML][HTML] Tumor necrosis factor α produces insulin resistance in skeletal muscle by activation of inhibitor κB kinase in a p38 MAPK-dependent manner
C de Alvaro, T Teruel, R Hernandez… - Journal of Biological …, 2004 - ASBMB
Insulin stimulation produced a reliable 3-fold increase in glucose uptake in primary neonatal
rat myotubes, which was accompanied by a similar effect on GLUT4 translocation to plasma
membrane. Tumor necrosis factor (TNF)-α caused insulin resistance on glucose uptake and
GLUT4 translocation by impairing insulin stimulation of insulin receptor (IR) and IR substrate
(IRS)-1 and IRS-2 tyrosine phosphorylation, IRS-associated phosphatidylinositol 3-kinase
activation, and Akt phosphorylation. Because this cytokine produced sustained activation of …
rat myotubes, which was accompanied by a similar effect on GLUT4 translocation to plasma
membrane. Tumor necrosis factor (TNF)-α caused insulin resistance on glucose uptake and
GLUT4 translocation by impairing insulin stimulation of insulin receptor (IR) and IR substrate
(IRS)-1 and IRS-2 tyrosine phosphorylation, IRS-associated phosphatidylinositol 3-kinase
activation, and Akt phosphorylation. Because this cytokine produced sustained activation of …