EFR3 and phosphatidylinositol 4-kinase IIIα regulate insulin-stimulated glucose transport and GLUT4 dispersal in 3T3-L1 adipocytes

Anna M. Koester, Angéline Geiser, Kamilla M.E. Laidlaw, Silke Morris, Marie F.A. Cutiongco, Laura Stirrat, Nikolaj Gadegaard, Eckhard Boles , Hannah L. Black, Nia J. Bryant, Gwyn W. Gould

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)
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Abstract

Insulin stimulates glucose transport in muscle and adipocytes. This is achieved by regulated delivery of intracellular glucose transporter (GLUT4)-containing vesicles to the plasmamembrane where they dock and fuse, resulting in increased cell surface GLUT4 levels. Recent work identified a potential further regulatory step, in which insulin increases the dispersal of GLUT4 in the plasmamembrane away from the sites of vesicle fusion. EFR3 is a scaffold protein that facilitates localization of phosphatidylinositol 4-kinase type IIIα to the cell surface. Here we show that knockdown of EFR3 or phosphatidylinositol 4-kinase type IIIα impairs insulin-stimulated glucose transport in adipocytes. Using direct stochastic reconstruction microscopy, we also show that EFR3 knockdown impairs insulin stimulated GLUT4 dispersal in the plasma membrane. We propose that EFR3 plays a previously unidentified role in controlling insulin-stimulated glucose transport by facilitating dispersal of GLUT4 within the plasma membrane.

Original languageEnglish
Article numberBSR20221181
Pages (from-to)1-13
Number of pages13
JournalBioscience Reports
Volume42
Issue number7
Early online date23 Jun 2022
DOIs
Publication statusPublished - 8 Jul 2022

Keywords

  • adipocytes
  • glucose transport
  • GLUT4
  • insulin

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