Bridging the GAP between insulin signaling and GLUT4 translocation

Robert T. Watson, Jeffrey E. Pessin

Research output: Contribution to journalArticle

158 Citations (Scopus)

Abstract

Upon binding and activating its cell-surface receptor, insulin triggers signaling cascades that regulate many cellular processes. Regarding glucose homeostasis, insulin suppresses hepatic glucose production and increases glucose transport into muscle and adipose tissues. At the cellular level, glucose uptake results from the insulin-stimulated translocation of the glucose transporter 4 (GLUT4) from intracellular storage sites to the plasma membrane. Although the signaling molecules that function proximal to the activated insulin receptor have been well characterized, it is not known how the distal insulin-signaling cascade interfaces with and mobilizes GLUT4-containing compartments. Recently, several candidate signaling molecules, including AS160, PIKfyve and synip, have been identified that might provide functional links between the insulin signaling cascade and GLUT4 compartments. Future work will focus on delineating the precise GLUT4 trafficking steps regulated by these molecules.

Original languageEnglish (US)
Pages (from-to)215-222
Number of pages8
JournalTrends in Biochemical Sciences
Volume31
Issue number4
DOIs
StatePublished - Apr 2006
Externally publishedYes

Fingerprint

Facilitative Glucose Transport Proteins
Insulin
Glucose
Molecules
Insulin Receptor
Cell Surface Receptors
Cell membranes
Muscle
Adipose Tissue
Homeostasis
Cell Membrane
Tissue
Muscles
Liver

ASJC Scopus subject areas

  • Biochemistry

Cite this

Bridging the GAP between insulin signaling and GLUT4 translocation. / Watson, Robert T.; Pessin, Jeffrey E.

In: Trends in Biochemical Sciences, Vol. 31, No. 4, 04.2006, p. 215-222.

Research output: Contribution to journalArticle

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