© 1999 American Heart Association, Inc.
Original Contribution |
Contribution of 
-Adrenergic and ß-Adrenergic Stimulation to Ischemia-Induced Glucose Transporter (GLUT) 4 and GLUT1 Translocation in the Isolated Perfused Rat Heart
From the Nuklearmedizinische Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universität München, Germany.
Correspondence to Silvia Egert, Nuklearmedizinische Klinik und Poliklinik, Technische Universität München, Ismaningerstr 22, 81675 München, Germany. E-mail Silvia.Egert{at}lrz.tu-muenchen.de
Abstract—The intracellular
signaling mechanism of the ischemia-stimulated glucose
transporter (GLUT) translocation in the heart is not yet characterized.
It has been suggested that catecholamines released during
ischemia may be involved in this pathway. The purpose of this
study was to evaluate the contribution of 
-adrenoceptors and
ß-adrenoceptors to ischemia-mediated GLUT4 and GLUT1
translocation in the isolated, Langendorff-perfused rat heart.
Additionally, GLUT translocation was studied in response to
catecholamine stimulation with phenylephrine
(Phy) and isoproterenol (Iso). The results were compared with
myocardial uptake of glucose analogue
[18F]fluorodeoxyglucose (FDG). Subcellular
analysis of GLUT4 and GLUT1 protein on plasma membrane vesicles
(PM) and intracellular membrane vesicles (IM) using membrane
preparation and immunoblotting revealed that - and
ß-receptor agonists stimulated GLUT4 translocation from IM to PM
(2.5-fold for Phy and 2.1-fold for Iso, P<0.05 versus
control), which was completely inhibited by phentolamine (Phe)
and propranolol (Pro), respectively.
Plasmalemmal GLUT1 moderately rose after Iso exposure, and
this was prevented by Pro. In contrast, ischemia-stimulated
GLUT4 translocation (2.2-fold, P<0.05 versus control)
was only inhibited by -adrenergic antagonist Phe but not
by ß-adrenergic antagonist Pro. Similarly, Phe but not
Pro inhibited ischemia-stimulated GLUT1 translocation. GLUT
data were confirmed by FDG uptake monitored using bismuth
germanate detectors. The catecholamine-stimulated
FDG uptake (6.9-fold for Phy and 8.9-fold for Iso) was significantly
inhibited by Phe and Pro; however, only Phe but not Pro significantly
reduced the ischemia-induced 2.5-fold increase in FDG uptake
(P<0.05 versus ischemia). This study suggests
that -adrenoceptor stimulation may play a role in the
ischemia-mediated increase in glucose transporter trafficking
leading to the stimulation of FDG uptake in the isolated, perfused rat
heart, whereas ß-adrenergic activation does not participate in this
signaling pathway.
Key Words: glucose transporter • ischemia • intracellular signaling • heart • catecholamine
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