Potential role of protein kinase B in glucose transporter 4 translocation in adipocytes

Phosphatidylinositol 3-kinase (PI 3-kinase) activation promotes glucose transporter 4 (Glut 4) translocation in adipocytes. In this study, we demonstrate that protein kinase B, a serine/threonine kinase stimulated by PI 3-kinase, is activated by both insulin and okadaic acid in isolated adipocytes,...

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Published inEndocrinology (Philadelphia) Vol. 138; no. 5; p. 2005
Main Authors Tanti, J F, Grillo, S, Grémeaux, T, Coffer, P J, Van Obberghen, E, Le Marchand-Brustel, Y
Format Journal Article
LanguageEnglish
Published United States 01.05.1997
Subjects
Adipocytes - metabolism
Animals
Biological Transport
Enzyme Activation - drug effects
Glucose Transporter Type 4
Immunoblotting
Immunosorbent Techniques
Insulin - pharmacology
Male
Monosaccharide Transport Proteins - metabolism
Muscle Proteins
Okadaic Acid - pharmacology
Phosphatidylinositol 3-Kinases
Phosphotransferases (Alcohol Group Acceptor) - metabolism
Platelet-Derived Growth Factor - pharmacology
Protein-Serine-Threonine Kinases
Proto-Oncogene Proteins - genetics
Proto-Oncogene Proteins - metabolism
Proto-Oncogene Proteins c-akt
Rats
Rats, Wistar
Transfection
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Summary:Phosphatidylinositol 3-kinase (PI 3-kinase) activation promotes glucose transporter 4 (Glut 4) translocation in adipocytes. In this study, we demonstrate that protein kinase B, a serine/threonine kinase stimulated by PI 3-kinase, is activated by both insulin and okadaic acid in isolated adipocytes, in parallel with their effects on Glut 4 translocation. In 3T3-L1 adipocytes, platelet-derived growth factor activated PI 3-kinase as efficiently as insulin but was only half as potent as insulin in promoting protein kinase B (PKB) activation. To look for a potential role of PKB in Glut 4 translocation, adipocytes were transfected with a constitutively active PKB (Gag-PKB) together with an epitope tagged transporter (Glut 4 myc). Gag-PKB was associated with all membrane fractions, whereas the endogenous PKB was mostly cytosolic. Expression of Gag-PKB led to an increase in Glut 4 myc amount at the cell surface. Our results suggest that PKB could play a role in promoting Glut 4 appearance at the cell surface following exposure of adipocytes to insulin and okadaic acid stimulation.
ISSN:0013-7227
DOI:10.1210/en.138.5.2005