Abstract
In this study, we demonstrated effects of acetyl-l-carnitine (ALC) on insulin resistance induced by tumor necrosis factor-alpha (TNF-alpha) in rat L6 cells. TNF-alpha downregulated insulin-stimulated glucose uptake and increased Serine 307 phosphorylation of insulin receptor substrate-1 (IRS-1). However, the treatment of ALC improved insulin-stimulated glucose uptake via AMP-activated protein kinase (AMPK) activation in a dose-dependent manner. Together, our data suggest that ALC inhibits TNF-alpha-induced insulin resistance through AMPK pathway in skeletal muscle cells.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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AMP-Activated Protein Kinases / metabolism*
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Acetylcarnitine / pharmacology*
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Animals
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Cell Line
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Glucose / metabolism
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Insulin / pharmacology
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Insulin Receptor Substrate Proteins / metabolism
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Insulin Resistance*
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Muscle, Skeletal / cytology
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Muscle, Skeletal / drug effects*
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Muscle, Skeletal / metabolism
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Phosphorylation
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Rats
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Serine / metabolism
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Tumor Necrosis Factor-alpha / antagonists & inhibitors*
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Tumor Necrosis Factor-alpha / pharmacology
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Tumor Necrosis Factor-alpha / physiology
Substances
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Insulin
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Insulin Receptor Substrate Proteins
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Irs1 protein, rat
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Tumor Necrosis Factor-alpha
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Serine
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Acetylcarnitine
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AMP-Activated Protein Kinases
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Glucose