Tomonori Takeuchi

A transgenic mutant mouse line accompanied by the complete deletion of interleukin-33 showed insulin and leptin resistances

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearch

  • Taku Watanabe
  • ,
  • Tomonori Takeuchi
  • Naoto Kubota
  • ,
  • Tasuku Wainai
  • ,
  • Keisuke Kataoka
  • ,
  • Toshitaka Nakaya
  • ,
  • Ayako Sugimoto
  • ,
  • Takahiro Sato
  • ,
  • Hiroshi Ohira
  • ,
  • Ichizo Tsujino
  • ,
  • Katsuyoshi Kumagai
  • ,
  • Tetsuya Kubota
  • ,
  • Chiaki Hasegawa
  • ,
  • Kumpei Tokuyama
  • ,
  • Kohjiro Ueki
  • ,
  • Toshimasa Yamauchi
  • ,
  • Masayoshi Mishina
  • ,
  • Takashi Kadowaki
Interleukin (IL) -33 has been identified as a member of the IL-1 family. Members of the IL-1 family have been reported to be involved in the regulation of energy homeostasis and glucose metabolism. Homozygous transgenic mutant mice of FLP14 line, that we previously generated, unexpectedly developed mature-onset obesity and diabetes. Through genetic investigations, we found that insertion of the transgenes had resulted in complete deletion of the Il33 gene. These obese male homozygous mutant mice exhibited hyperphagia with hyperleptinemia and insulin resistance caused by increased hepatic gluconeogenesis and decreased glucose uptake in skeletal muscle. As a result of examining preobese male homozygous mutant mice to investigate with the exclusion of the effect of obesity, hyperphagia with hyperleptinemina and insulin resistance caused by decreased glucose uptake in skeletal muscle were already observed, but the increased hepatic glucose production was not. To investigate whether the insulin resistance was caused by deletion of the Il33 gene, we treated these preobese homozygous mutant mice with recombinant IL-33 protein and noted a significant improvement in insulin resistance. Thus, insulin resistance in these homozygous mutant mice was caused, at least in part, by IL-33 deficiency, suggesting a favorable role of IL-33 for glucose metabolism in the skeletal muscle.
Original languageEnglish
JournalbioRxiv
Publication statusPublished - 2018

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