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Curr Opin Cell Biol. 2010 Aug;22(4):506-12. doi: 10.1016/j.ceb.2010.03.012. Epub 2010 Apr 21.

Biogenesis and regulation of insulin-responsive vesicles containing GLUT4.

Author information

1
Section of Endocrinology and Metabolism, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA. jonathan.bogan@yale.edu

Abstract

Insulin regulates the trafficking of GLUT4 glucose transporters in fat and muscle cells. In unstimulated cells, GLUT4 is sequestered intracellularly in small, insulin-responsive vesicles. Insulin stimulates the translocation of these vesicles to the cell surface, inserting the transporters into the plasma membrane to enhance glucose uptake. Formation of the insulin-responsive vesicles requires multiple interactions among GLUT4, IRAP, LRP1, and sortilin, as well as recruitment of GGA and ACAP1 adaptors and clathrin. Once formed, the vesicles are retained within unstimulated cells by the action of TUG, Ubc9, and other proteins. In addition to acting at other steps in vesicle recycling, insulin releases this retention mechanism to promote the translocation and fusion of the vesicles at the cell surface.

PMID:
20417083
PMCID:
PMC2910140
DOI:
10.1016/j.ceb.2010.03.012
[Indexed for MEDLINE]
Free PMC Article
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