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1 Department of Surgery, Huddinge University Hospital, S-141 86 Huddinge; Departments of 3 Surgery and 4 Thoracic Clinical Physiology, Karolinska Hospital and Karolinska Institute, S-17177 Stockholm, Sweden; and 2 Joslin Diabetes Center and Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02215
Studies in rodents have established that GLUT-4
translocation is the major mechanism by which insulin and exercise
increase glucose uptake in skeletal muscle. In contrast, much less is
known about the translocation phenomenon in human skeletal muscle. In the current study, nine healthy volunteers were studied on two different days. On one day, biopsies of vastus lateralis muscle were
taken before and after a 2-h euglycemic-hyperinsulinemic clamp (0.8 mU · kg
1 · min1).
On another day, subjects exercised for 60 min at 70% of maximal oxygen
consumption (
O2 max),
a biopsy was obtained, and the same clamp and biopsy procedure was
performed as that during the previous experiment. Compared with insulin
treatment alone, glucose infusion rates were significantly increased
during the postexercise clamp for the periods 0-30 min, 30-60
min, and 60-90 min, but not during the last 30 min of the clamp.
Plasma membrane GLUT-4 content was significantly increased in response
to physiological hyperinsulinemia (32% above rest), exercise (35%),
and the combination of exercise plus insulin (44%). Phosphorylation of
Akt, a putative signaling intermediary for GLUT-4 translocation, was
increased in response to insulin (640% above rest), exercise (280%),
and exercise plus insulin (1,000%). These data demonstrate that two normal physiological conditions, moderate intensity exercise and physiological hyperinsulinemia ~56 µU/ml, cause GLUT-4
translocation and Akt phosphorylation in human skeletal muscle.
glucose transporters; glucose uptake; Akt; glucose disposal; muscle contraction
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