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

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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 α 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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Acknowledgment

This work was supported in part by the National Natural Science Foundation of China (No.30400216), Shanghai-SK Research and Development Fund (2003007-t), Shanghai Excellent Youth Doctor (2004), Shanghai Youth Star of Science and Technology (05QMX1430).

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Authors and Affiliations

  1. Department of Endocrinology and Metabolism, Shanghai Clinical Center for Endocrine & Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao-Tong University Medical School, 197 Rui-Jin 2nd Road, Shanghai, 200025, China

    Yi-Sheng Yang, Xiao-Ying Li, Jie Hong, Wei-Qiong Gu, Yi-Fei Zhang, Jun Yang, Jia-Lun Chen & Guang Ning

  2. State Key Laboratory of Medical Genomics, Rui-Jin Hospital, Shanghai Jiao-Tong University Medical School, 197 Rui-Jin 2nd Road, Shanghai, 200025, China

    Huai-Dong Song

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  1. Yi-Sheng Yang
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  4. Wei-Qiong Gu
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  9. Guang Ning
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Correspondence to Guang Ning.

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Yang, YS., Li, XY., Hong, J. et al. Interleukin-18 enhances glucose uptake in 3T3-L1 adipocytes. Endocr 32, 297–302 (2007). https://doi.org/10.1007/s12020-008-9048-z

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  • DOI: https://doi.org/10.1007/s12020-008-9048-z

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