Acetylation of TUG protein promotes the accumulation of GLUT4 glucose transporters in an insulin-responsive intracellular compartment

Abstract

Background: Insulin stimulates glucose uptake by triggering TUG proteolysis, which liberates intracellular storage vesicles containing GLUT4. Results:TUGacetylation modulates its interaction with Golgi matrix proteins and enhances its function to trap GLUT4 storage vesicles within unstimulated cells. SIRT2 modulates TUG acetylation and controls insulin sensitivity in vivo. Conclusion: TUG acetylation promotes GLUT4 accumulation in insulin-responsive vesicles. Significance: Nutritional status modulates insulin-stimulated glucose uptake.