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1998 Fiscal Year Final Research Report Summary

Stracture and Function of glucose transporters using myc-tag.

Research Project

Project/Area Number 09680595
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Structural biochemistry
Research InstitutionThe University of Tokushima

Principal Investigator

WANG Lihong  The University of Tokushima Institute for Enzyme Research, Research Associate, 分子酵素学研究センター, 助手 (40284319)

Co-Investigator(Kenkyū-buntansha) KISHI Kazuhiro  The University of Tokushima Institute for Enzyme Research, Research Associate, 分子酵素学研究センター, 助手 (70284320)
Project Period (FY) 1997 – 1998
KeywordsGlucose transporter / Insulin Action / PDGF / Translocation
Research Abstract

We earlier developed a novel method to detect translocation of the glucose transporter (GLUT), derectly and simply using c-myc epitopr-tagged GLUT (GLUTmyc). To define the effect of platelet-derived growth factor (PDGF) on glucose transport in 3T3-L1 adipocytes, we investigated the PDGF- and insulin-induced glucose uptake, translocation of glucose uptake by 9-10-fold and 5.5-6.5-fold, respectively, in both 3T3-L1 and 3T3-L1GLUT4myc adipocytes. Exogenous GLUT4myc expression led to enhanced PDGF-induced glucose transport. In 3T3-L1GLUT4myc adipocytes, insulin and PDGF induced an 3-fold and 5-fold increase in GLUT4myc translocation, respectively, determined in a cell surface anti-c-myc antibody binding assay. This PDGF-induced GLUT4myc translocation was further demonstrated with fluorescent detection. In contrast, PDGF stimulated a 2-fold increase of GLUT1myc translcoation and 2.5-fold increase of glucose uptake in 3T3-L1GLUT1myc adipocytes. The PDGF-induced GLUT4myc translocation, glucose uptake and PI 3-kinase activity were maximal (100%) at 5-10 min, and thereafter rapidly declined to 40%, 30%, and 18%, respectively, within 60 min, a time when effects of insulin were maximal. Wortmannin (0.1 mM) abolished PDGF-induced GLUT4myc translocation and glucose uptake in 3T3-L1GLUT4myc adipocytes. These results suggest that PDGF can transiently trigger the trasnlocation of GLUT4 and stimulates glucose uptake by translocation of both GLUT4 and GLUT1 in a phosphatidylinositol 3-kinase-dependent signaling pathway in 3T3-L1 adipocytes.

  • Research Products

    (4 results)

All Other

All Publications (4 results)

  • [Publications] Takanobu Imanaka,Wang Lihong,Yousuke Ebina,et al.: "Reconatitution of Insulin Signaling Pathways in Rat 3Y1 Cells Lacking Insulin Receptor and Insulin Receptor Substrate-1" J.Biol.Chem.273. 25347-25355 (1998)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Wang Lihong,Yousuke Ebina,et al.: "Hyperinsulinemia but no diabetes in transgenic mice homozygously expressing the tyrosine kinase-deficient human insulin receptor" Biochem.Biophys.Res.Commun.240. 446-451 (1997)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Imanaka T., Wang L., Ebina Y.et.al.: "Reconatitution of Insluin Signaling Pathway in Rat3Yl Cells lacking Insulin Receptor and Insulin Receptor Substrate-1" J.Biol.Chem.273. 25347-25355 (1998)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Wang L., Ebina Y.et.al: "Hyperinsulinemia but no diabetes in transgenic mice homozygously expressing the tyrosine kinase-deficient human insulin receptor" Biochem.Biophys.Res Commun.240. 446-451 (1997)

    • Description
      「研究成果報告書概要(欧文)」より

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Published: 1999-12-08  

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