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

by: Yi-Sheng S Yang, Xiao-Ying Y Li, Jie Hong, Wei-Qiong Q Gu, Yi-Fei F Zhang, Jun Yang, Huai-Dong D Song, Jia-Lun L Chen, Guang Ning
Endocrine, Vol. 32, No. 3. (December 2007), pp. 297-302.


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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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