Interleukin-18 enhances glucose uptake in 3T3-L1 adipocytes.
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.
Yang
Yi-Sheng
YS
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, Shanghai 200025, China.
Li
Xiao-Ying
XY
Hong
Jie
J
Gu
Wei-Qiong
WQ
Zhang
Yi-Fei
YF
Yang
Jun
J
Song
Huai-Dong
HD
Chen
Jia-Lun
JL
Ning
Guang
G
D041721:3T3-L1 Cells / Q000166:cytology / Q000378:metabolism*; D017667:Adipocytes / Q000166:cytology / Q000378:metabolism*; D000818:Animals; D002478:Cells, Cultured; D015536:Down-Regulation; D005947:Glucose / Q000493:pharmacokinetics*; D007333:Insulin Resistance / Q000502:physiology; D020382:Interleukin-18 / Q000378:metabolism / Q000502:physiology*; D051379:Mice; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism; D053724:Receptors, Interleukin-18 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015854:Up-Regulation; D048051:p38 Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism
D020382:Interleukin-18; D053724:Receptors, Interleukin-18; D014409:Tumor Necrosis Factor-alpha; D051057:Proto-Oncogene Proteins c-akt; D048051:p38 Mitogen-Activated Protein Kinases; D005947:Glucose