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• W1923643609 endingPage "E855" @default.
• W1923643609 startingPage "E849" @default.
• W1923643609 abstract "Physiological stressors such as sepsis and tissue damage initiate an acute immune response and cause transient systemic insulin resistance. This study was conducted to determine whether tumor necrosis factor-α (TNF-α), a cytokine produced by immune cells during skeletal muscle damage, decreases insulin responsiveness at the cellular level. To examine the molecular mechanisms associated with TNF-α and insulin action, we measured insulin receptor substrate (IRS)-1- and IRS-2-mediated phosphatidylinositol 3-kinase (PI 3-kinase) activation, IRS-1-PI 3-kinase binding, IRS-1 tyrosine phosphorylation, and the phosphorylation of two mitogen-activated protein kinases (MAPK, known as p42 MAPK and p44 MAPK ) in cultured C 2 C 12 myotubes. Furthermore, we determined the effects of TNF-α on insulin-stimulated 2-deoxyglucose (2-DG) uptake. We observed that TNF-α impaired insulin stimulation of IRS-1- and IRS-2-mediated PI 3-kinase activation by 54 and 55% ( P< 0.05), respectively. In addition, TNF-α decreased insulin-stimulated IRS-1 tyrosine phosphorylation by 40% ( P < 0.05). Furthermore, TNF-α repressed insulin-induced p42 MAPK and p44 MAPK tyrosine phosphorylation by 81% ( P < 0.01). TNF-α impairment of insulin signaling activation was accompanied by a decrease ( P < 0.05) in 2-DG uptake in the muscle cells (60 ± 4 vs. 44 ± 6 pmol ⋅ min −1 ⋅ mg −1 ). These data suggest that increases in TNF-α may cause insulin resistance in skeletal muscle by inhibiting IRS-1- and IRS-2-mediated PI 3-kinase activation as well as p42 MAPK and p44 MAPK tyrosine phosphorylation, leading to impaired insulin-stimulated glucose uptake." @default.
• W1923643609 created "2016-06-24" @default.
• W1923643609 creator A5029909577 @default.
• W1923643609 creator A5032996365 @default.
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• W1923643609 date "1999-05-01" @default.
• W1923643609 modified "2023-10-06" @default.
• W1923643609 title "TNF-α impairs insulin signaling and insulin stimulation of glucose uptake in C₂C₁₂muscle cells" @default.
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• W1923643609 doi "https://doi.org/10.1152/ajpendo.1999.276.5.e849" @default.
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