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Rab10, a Target of the AS160 Rab GAP, Is Required for Insulin-Stimulated Translocation of GLUT4 to the Adipocyte Plasma Membrane

Sano, Hiroyuki, Eguez, Lorena, Teruel, Mary N., Fukuda, Mitsunori, Chuang, Tuan D., Chavez, Jose A., Lienhard, Gustav E., McGraw, Timothy E.·2007·Cell Metabolism
DOI 10.1016/j.cmet.2007.03.001
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Abstract

GLUT4 trafficking to the plasma membrane of muscle and fat cells is regulated by insulin. An important component of insulin-regulated GLUT4 distribution is the Akt substrate AS160 rab GTPase-activating protein. Here we show that Rab10 functions as a downstream target of AS160 in the insulin-signaling pathway that regulates GLUT4 translocation in adipocytes. Overexpression of a mutant of Rab10 defective for GTP hydrolysis increased GLUT4 on the surface of basal adipocytes. Rab10 knockdown resulted in an attenuation of insulin-induced GLUT4 redistribution to the plasma membrane and a concomitant 2-fold decrease in GLUT4 exocytosis rate. Re-expression of a wild-type Rab10 restored normal GLUT4 translocation. The basal increase in plasma-membrane GLUT4 due to AS160 knockdown was partially blocked by knocking down Rab10 in the same cells, further indicating that Rab10 is a target of AS160 and a positive regulator of GLUT4 trafficking to the cell surface upon insulin stimulation.

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Metadata

Authors
Sano, H., Eguez, L., Teruel, M. N., Fukuda, M., Chuang, T. D., Chavez, J. A., Lienhard, G. E., & McGraw, T. E.
Venue
Cell Metabolism
Publisher
Elsevier BV
Published
2007-04
Volume
5
Issue
4
Pages
293-303
ISSN
1550-4131
DOI
10.1016/j.cmet.2007.03.001
Cited by
340
References
2
Language
en
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