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Interleukin-18 enhances glucose uptake in 3T3-L1 adipocytes
Authors:Yang Yi-Sheng  Li Xiao-Ying  Hong Jie  Gu Wei-Qiong  Zhang Yi-Fei  Yang Jun  Song Huai-Dong  Chen Jia-Lun  Ning Guang
Institution:(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;(2) State Key Laboratory of Medical Genomics, Rui-Jin Hospital, Shanghai Jiao-Tong University Medical School, 197 Rui-Jin 2nd Road, Shanghai, 200025, China
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.
Keywords:Interleukin-18  Insulin resistance  3T3-L1 adipocytes  Adipokines  p38 MAPK
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