| Literature DB >> 18247160 |
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.Entities:
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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