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J Biol Chem, Vol. 274, Issue 25, 17934-17940, June 18, 1999
From the To characterize the contribution of glycogen
synthase kinase 3
The Role of Glycogen Synthase Kinase 3
in Insulin-stimulated
Glucose Metabolism
,,
Howard Hughes Medical Institute, University
of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, the § Department of Physiology and Biophysics, University of
Iowa College of Medicine, Iowa City, Iowa 52242, and the
¶ Department of Molecular Pharmacology, Stanford University School
of Medicine, Stanford, California 94305
(GSK3) inactivation to insulin-stimulated
glucose metabolism, wild-type (WT-GSK), catalytically inactive
(KM-GSK), and uninhibitable (S9A-GSK) forms of GSK3 were expressed
in insulin-responsive 3T3-L1 adipocytes using adenovirus technology.
WT-GSK, but not KM-GSK, reduced basal and insulin-stimulated glycogen
synthase activity without affecting the -fold stimulation of the enzyme by insulin. S9A-GSK similarly decreased cellular glycogen synthase activity, but also partially blocked insulin stimulation of the enzyme.
S9A-GSK expression also markedly inhibited insulin stimulation of
IRS-1-associated phosphatidylinositol 3-kinase activity, but only
weakly inhibited insulin-stimulated Akt/PKB phosphorylation and glucose
uptake, with no effect on GLUT4 translocation. To further evaluate the
role of GSK3 in insulin signaling, the GSK3 inhibitor lithium was
used to mimic the consequences of insulin-stimulated GSK3
inactivation. Although lithium stimulated the incorporation of glucose
into glycogen and glycogen synthase enzyme activity, the inhibitor was
without effect on GLUT4 translocation and pp70 S6 kinase. Lithium
stimulation of glycogen synthesis was insensitive to wortmannin, which
is consistent with its acting directly on GSK3 downstream of
phosphatidylinositol 3-kinase. These data support the hypothesis that
GSK3 contributes to insulin regulation of glycogen synthesis, but is
not responsible for the increase in glucose transport.
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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