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Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110
The purpose of this study was to determine
whether the increase in insulin sensitivity of skeletal muscle glucose
transport induced by a single bout of exercise is mediated by enhanced
translocation of the GLUT-4 glucose transporter to the cell surface.
The rate of
3-O-[3H]methyl-D-glucose
transport stimulated by a submaximally effective concentration of
insulin (30 µU/ml) was approximately twofold greater in the muscles
studied 3.5 h after exercise than in those of the sedentary controls
(0.89 ± 0.10 vs. 0.43 ± 0.05 µmol · ml
1 · 10 min1; means ± SE for
n = 6/group). GLUT-4 translocation was
assessed by using the
ATB-[2-3H]BMPA
exofacial photolabeling technique. Prior exercise resulted in greater
cell surface GLUT-4 labeling in response to submaximal insulin
treatment (5.36 ± 0.45 dpm × 103/g in exercised vs. 3.00 ± 0.38 dpm × 103/g in
sedentary group; n = 10/group) that
closely mirrored the increase in glucose transport activity. The signal
generated by the insulin receptor, as reflected in the extent of
insulin receptor substrate-1 tyrosine phosphorylation, was unchanged
after the exercise. We conclude that the increase in muscle insulin
sensitivity of glucose transport after exercise is due to translocation
of more GLUT-4 to the cell surface and that this effect is not due to
potentiation of insulin-stimulated tyrosine phosphorylation.
insulin receptor; insulin receptor substrate-1; tyrosine phosphorylation
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