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J. Biol. Chem., Vol. 269, Issue 28, 18366-18370, Jul, 1994
EA Gulve, JM Ren, BA Marshall, J Gao, PA Hansen, JO Holloszy and M Mueckler
Glucose transport activity was examined in transgenic mice overexpressing
the human GLUT1 glucose transporter in skeletal muscles. Basal transport
activity measured in vitro with the glucose analog 2- deoxy-D-glucose (1
mM) was increased 2-8-fold in four different muscle preparations.
Incubation of muscles from control nontransgenic littermates with a
maximally effective concentration of insulin or with insulin-like growth
factor-1 resulted in glucose transport rates that were 2-3-fold higher than
basal. In contrast, insulin did not stimulate glucose transport activity in
three different muscle preparations from transgenic animals; insulin-like
growth factor-1 was similarly ineffective. Activation of System A amino
acid transport activity (measured with the nonmetabolizable analog alpha-
methylaminoisobutyrate) by insulin was not impaired in muscles from
transgenic mice, indicating that the defect does not involve the insulin
receptor. In skeletal muscle, glucose transport can be activated by muscle
contractions or hypoxia via a pathway separate from that activated by
insulin. Incubation of muscles under hypoxic conditions or stimulation of
muscles to contract in situ did not increase glucose transport activity in
muscles from GLUT1- overexpressing mice, in contrast to the stimulatory
effects measured in muscles from control animals. These data suggest that
increased glucose flux per se into skeletal muscle results in resistance of
GLUT4 to activation by insulin and various other stimuli that activate
glucose transport by mechanisms distinct from that of insulin. GLUT1-
overexpressing mice thus provide a new model system for studying the
effects of glucose-induced resistance to activation of glucose transport.
Glucose transport activity in skeletal muscles from transgenic mice overexpressing GLUT1. Increased basal transport is associated with a defective response to diverse stimuli that activate GLUT4
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110.
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