HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

J. Biol. Chem., Vol. 280, Issue 38, 32625-32633, September 23, 2005

This Article Full Text Full Text (PDF) All Versions of this Article: 280/38/32625    most recent M507221200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ferreira, I. A. Articles by Akkerman, J.-W. N. Search for Related Content PubMed PubMed Citation Articles by Ferreira, I. A. Articles by Akkerman, J.-W. N. Social Bookmarking                      What's this?

Glucose Uptake via Glucose Transporter 3 by Human Platelets Is Regulated by Protein Kinase B^*

From the Thrombosis and Haemostasis Laboratory, Department of Hematology, University Medical Center Utrecht, and the Institute for Biomembranes, Utrecht University, HP G03.647, Heidelberglaan 100, Utrecht 3584 CX, the Netherlands

In insulin-responsive tissues, insulin is a potent activator of protein kinase B (PKB)-mediated glucose uptake through the facilitative glucose transporter GLUT4. In platelets, glucose uptake is mediated through GLUT3, which is present in plasma (15%) and intracellular -granule (85%) membranes. Here we report the PKB-mediated glucose uptake by platelets by agents that do (thrombin) or do not (insulin) induce -granule translocation to the plasma membrane. Both thrombin and insulin activate PKB and induce glucose uptake albeit with different kinetics. Inhibition of PKB by the pharmacological inhibitor ML-9 decreases thrombin-induced -granule release and thrombin- and insulin-induced glucose uptake. At low glucose (0.1 mM), both agents stimulate glucose uptake by lowering the K_m for glucose (thrombin and insulin) and increasing V_max (thrombin). At high glucose (5 mM), stimulation of glucose uptake by insulin disappears, and insulin becomes an inhibitor of thrombin-induced glucose uptake via mechanisms independent of PKB. We conclude that in platelets glucose transport through GLUT3 is regulated by changes in surface expression and affinity modulation, which are both under control of PKB.

Received for publication, July 5, 2005

^* This work was supported in part by the Dutch Diabetes Research Foundation (Grant 1999.046) and the Fonds voor het Hart. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Supported by the Dutch Thrombosis Foundation. To whom correspondence should be addressed. Tel.: 31-30-250-6512; Fax: 31-30-251-1893; E-mail: j.w.n.akkerman{at}azu.nl.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				I. A. Simpson, D. Dwyer, D. Malide, K. H. Moley, A. Travis, and S. J. Vannucci The facilitative glucose transporter GLUT3: 20 years of distinction Am J Physiol Endocrinol Metab, August 1, 2008; 295(2): E242 - E253. [Abstract] [Full Text] [PDF]

				H. M.W. Verheul, M. P.J. Lolkema, D. Z. Qian, Y. H.A. Hilkes, E. Liapi, J.-W. N. Akkerman, R. Pili, and E. E. Voest Platelets Take Up the Monoclonal Antibody Bevacizumab Clin. Cancer Res., September 15, 2007; 13(18): 5341 - 5347. [Abstract] [Full Text] [PDF]

				I. A. Ferreira, A. I.M. Mocking, M. A.H. Feijge, G. Gorter, T. W. van Haeften, J. W.M. Heemskerk, and J.-W. N. Akkerman Platelet Inhibition by Insulin Is Absent in Type 2 Diabetes Mellitus Arterioscler. Thromb. Vasc. Biol., February 1, 2006; 26(2): 417 - 422. [Abstract] [Full Text] [PDF]