Abstract
In order to characterize the potential causative effects of interleukin-18 (IL-18) on insulin resistance, we measured glucose uptake in 3T3-L1 adipocytes treated with mouse recombinant IL-18. IL-18 surprisingly enhanced, rather than reduced insulin-mediated glucose uptake in adipocytes. Moreover IL-18 could counteract the glucose uptake suppression caused by tumor necrosis factor alpha in 3T3-L1 adipocytes. The mechanism dissection showed that the IL-18 upregulated phosphorylated Akt and downregulated phosphorylated P38 MAPK. These findings indicated that the elevated serum IL-18 levels in obesity and diabetes might be a compensatory response to insulin resistance.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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3T3-L1 Cells / cytology
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3T3-L1 Cells / metabolism*
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Adipocytes / cytology
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Adipocytes / metabolism*
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Animals
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Cells, Cultured
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Down-Regulation
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Glucose / pharmacokinetics*
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Insulin Resistance / physiology
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Interleukin-18 / metabolism
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Interleukin-18 / physiology*
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Mice
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Proto-Oncogene Proteins c-akt / genetics
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Proto-Oncogene Proteins c-akt / metabolism
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Receptors, Interleukin-18 / metabolism
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Tumor Necrosis Factor-alpha / metabolism
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Up-Regulation
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p38 Mitogen-Activated Protein Kinases / genetics
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p38 Mitogen-Activated Protein Kinases / metabolism
Substances
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Interleukin-18
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Receptors, Interleukin-18
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Tumor Necrosis Factor-alpha
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Proto-Oncogene Proteins c-akt
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p38 Mitogen-Activated Protein Kinases
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Glucose