Insulin and nonhydrolyzable GTP analogs induce translocation of GLUT 4 to the plasma membrane in α-toxin-permeabilized rat adipose cells

G. Baldini, R. Hohman, M. J. Charron, H. F. Lodish

Research output: Contribution to journalArticle

114 Scopus citations

Abstract

Rat adipose cells treated with Staphylococcus aureus α-toxin are permeable and retain their ability to respond to insulin after hormone treatment. The GLUT 4 glucose transporter isoform, specific to fat and muscle cells, is translocated normally from low density microsomes to the plasma membrane in permeabilized cells. Addition of guanosine 5'-O-(3-thiotriphosphate), guanylyl imidodiphosphate, or guanylyl β,γ-methylenediphosphate to permeabilized adipocytes induces an insulin-like translocation of GLUT 4 to the plasma membrane; GTP or adenosine 5'-(β,γ-imino)triphosphate has no effect. No translocation of GLUT 4 is observed when GTP analogs are added to intact adipocytes. These results suggest the involvement of a GTP-binding protein in insulin-triggered recruitment of GLUT 4 to the cell surface.

Original languageEnglish (US)
Pages (from-to)4037-4040
Number of pages4
JournalJournal of Biological Chemistry
Volume266
Issue number7
StatePublished - Jul 18 1991

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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