ID 25669
Author
Noda, Satoshi Department of Radiology, The University of Tokushima School of Medicine
Kishi, Kazuhiro Division of Molecular Genetics, Institute for Enzyme Research, The University of Tokushima
Yuasa, Tomoyuki Division of Molecular Genetics, Institute for Enzyme Research, The University of Tokushima Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Hayashi, Hideki Division of Molecular Genetics, Institute for Enzyme Research, The University of Tokushima
Ohnishi, Tetsuo Division of Molecular Genetics, Institute for Enzyme Research, The University of Tokushima
Miyata, Ikuko Division of Molecular Genetics, Institute for Enzyme Research, The University of Tokushima
Nishitani, Hiromu Department of Radiology, The University of Tokushima School of Medicine Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Ebina, Yousuke Division of Molecular Genetics, Institute for Enzyme Research, The University of Tokushima Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Keywords
AKT
p70S6 kinase
GSK3β
GLUT4
Content Type
Journal Article
Description
We have developed a simple, direct and sensitive method to detect GLUT4 on the cell surface. Using this system, we found that PI3-kinase plays a key role in the signaling pathway of insulin-stimulated GLUT4 translocation. One of the down stream effectors of PI3-kinase is serine-threonine kinase Akt (protein kinase B, RAK-PK), but the involvement of Akt in insulin-stimulated GLUT4 translocation is controversial. To investigate whether Akt1 regulates insulin-stimulated GLUT4 translocation and glucose uptake in L6 myotubes, we established L6 myotubes stably expressing c-myc epitope-tagged GLUT4 (GLUT4myc) and mouse wild type (WT) Akt1. We found that overexpression of WT Akt1 promoted insulin-stimulated p70S6 kinase (p70S6K) activity and increased the basal activity of GSK3β, but did not promote insulin-stimulated GLUT4translocation or glucose uptake. These data supported the result that Akt is not a main signaling molecule to transmit the signal of insulin-stimulated GLUT4 translocation or glucose uptake from insulin-activated PI3-kinase.
Journal Title
The journal of medical investigation : JMI
ISSN
13431420
NCID
AA11166929
Volume
47
Issue
1-2
Start Page
47
End Page
55
Sort Key
47
Published Date
2000
Remark
EDB ID
FullText File
language
eng
departments
Medical Sciences
Institute of Advanced Medical Sciences