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

Endocrine. 2007 Dec;32(3):297-302. doi: 10.1007/s12020-008-9048-z. Epub 2008 Feb 5.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells / cytology
  • 3T3-L1 Cells / metabolism*
  • Adipocytes / cytology
  • Adipocytes / metabolism*
  • Animals
  • Cells, Cultured
  • Down-Regulation
  • Glucose / pharmacokinetics*
  • Insulin Resistance / physiology
  • Interleukin-18 / metabolism
  • Interleukin-18 / physiology*
  • Mice
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism
  • Receptors, Interleukin-18 / metabolism
  • Tumor Necrosis Factor-alpha / metabolism
  • Up-Regulation
  • p38 Mitogen-Activated Protein Kinases / genetics
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Interleukin-18
  • Receptors, Interleukin-18
  • Tumor Necrosis Factor-alpha
  • Proto-Oncogene Proteins c-akt
  • p38 Mitogen-Activated Protein Kinases
  • Glucose