Ethanol feeding induces insulin resistance with enhanced PI 3-kinase activation

Yukiko Onishi, Miho Honda, Takehide Ogihara, Hideyuki Sakoda, Motonobu Anai, Midori Fujishiro, Hiraku Ono, Nobuhiro Shojima, Yasushi Fukushima, Kouichi Inukai, Hideki Katagiri, Masatoshi Kikuchi, Yoshitomo Oka, Tomoichiro Asano

Research output: Contribution to journalArticlepeer-review

83 Citations (Scopus)


High ethanol intake is considered to impair insulin sensitivity. In the present study, we investigated the acute and chronic effects of ethanol intake on glucose metabolism and insulin signal transduction. Hyperinsulinemic-euglycemic clamp studies revealed 70% and 51% decreases in the glucose infusion rate, 52% and 31% decreases in the glucose utilization rate, and 6.6- and 8.0-fold increases in hepatic glucose in continuous- and acute-ethanol-loaded rats, respectively. Despite the presence of insulin resistance, alcohol-fed rats showed enhanced tyrosine phosphorylation of insulin receptors, IRS-1 and IRS-2, induced by insulin injection via the portal vein. PI 3-kinase activities associated with IRSs and phosphotyrosine also increased significantly as compared with those of controls. These data suggest ethanol intake to be a factor leading to insulin resistance, regardless of whether it is a single or continuous intake. In addition, the insulin signaling step impaired by ethanol feeding is likely to be downstream from PI 3-kinase.

Original languageEnglish
Pages (from-to)788-794
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number3
Publication statusPublished - 2003 Apr 11


  • Ethanol
  • Euglycemic-hyperinsulinemic clamp study
  • Insulin resistance
  • Insulin signaling
  • Phosphatidylinositol 3-kinase


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