Regulated Membrane Trafficking of the Insulin-Responsive Glucose Transporter 4 in Adipocytes
Robert T. Watson,
Makoto Kanzaki and
Jeffrey E. Pessin
Department of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, New York 11794
Correspondence: Address all correspondence and requests for reprints to: Jeffrey E. Pessin, Ph.D., Department of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, New York 11794. E-mail: pessin{at}pharm.sunysb.edu
Since the discovery of insulin roughly 80 yr ago, much has beenlearned about how target cells receive, interpret, and respondto this peptide hormone. For example, we now know that insulinactivates the tyrosine kinase activity of its cell surface receptor,thereby triggering intracellular signaling cascades that regulatemany cellular processes. With respect to glucose homeostasis,these include the function of insulin to suppress hepatic glucoseproduction and to increase glucose uptake in muscle and adiposetissues, the latter resulting from the translocation of theglucose transporter 4 (GLUT4) to the cell surface membrane.Although simple in broad outline, elucidating the molecularintricacies of these receptor-signaling pathways and membrane-traffickingprocesses continues to challenge the creative ingenuity of scientists,and many questions remain unresolved, or even perhaps unasked.The identification and functional characterization of specificmolecules required for both insulin signaling and GLUT4 vesicletrafficking remain key issues in our pursuit of developing specifictherapeutic agents to treat and/or prevent this debilitatingdisease process. To this end, the combined efforts of numerousresearch groups employing a range of experimental approacheshas led to a clearer molecular picture of how insulin regulatesthe membrane trafficking of GLUT4.
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