Insulin Stimulates Actin Comet Tails on Intracellular GLUT4-containing Compartments in Differentiated 3T3L1 Adipocytes* 210

Incubation of isolated GLUT4-containing vesicles with Xenopus oocyte extracts resulted in a guanosine 5′-[γ-thio]triphosphate (GTPγS) and sodium orthovanadate stimulation of actin comet tails. The in vitro actin-based GLUT4 vesicle motility was inhibited by both latrunculin B and a dominant-interfering N-WASP mutant, N-WASP/ΔVCA. Preparations of gently sheared (broken) 3T3L1 adipocytes also displayed GTPγS and sodium orthovanadate stimulation of actin comet tails on GLUT4 intracellular compartments. Furthermore, insulin pretreatment of intact adipocytes prior to gently shearing also resulted in a marked increase in actin polymerization and actin comet tailing on GLUT4 vesicles. In addition, the insulin stimulation of actin comet tails was completely inhibited by Clostridum difficile toxin B, demonstrating a specific role for a Rho family member small GTP-binding protein. Expression of N-WASP/ΔVCA in intact cells had little effect on adipocyte cortical actin but partially inhibited insulin-stimulated GLUT4 translocation. Taken together, these data demonstrate that insulin can induce GLUT4 vesicle actin comet tails that are necessary for the efficient translocation of GLUT4 from intracellular storage sites to the plasma membrane.

• Publication year

  2001

• Venue

  Journal of Biological Chemistry

• Publication date

  2001-12-28

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1074/JBC.M109657200PMID 11606595
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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