Literature DB >> 18247160

Interleukin-18 enhances glucose uptake in 3T3-L1 adipocytes.

Yi-Sheng Yang1, Xiao-Ying Li, Jie Hong, Wei-Qiong Gu, Yi-Fei Zhang, Jun Yang, Huai-Dong Song, Jia-Lun Chen, Guang Ning.   

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.

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Year:  2008        PMID: 18247160     DOI: 10.1007/s12020-008-9048-z

Source DB:  PubMed          Journal:  Endocrine        ISSN: 1355-008X            Impact factor:   3.633


  29 in total

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7.  Pharmacological inhibition of p38 MAP kinase results in improved glucose uptake in insulin-resistant 3T3-L1 adipocytes.

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9.  Tumor necrosis factor alpha rapidly activates the mitogen-activated protein kinase (MAPK) cascade in a MAPK kinase kinase-dependent, c-Raf-1-independent fashion in mouse macrophages.

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Review 3.  Role of Inflammatory Cytokines, Growth Factors and Adipokines in Adipogenesis and Insulin Resistance.

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  5 in total

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