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Exerciseand insulin cause GLUT-4 translocation in human skeletal muscle

Thorell, Anders (författare)
Department of Surgery, Huddinge University Hospital, Huddinge, Sweden
Hirshman, Michael F. (författare)
Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA, United States
Nygren, Jonas O. (författare)
Department of Surgery, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden
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Jorfeldt, Lennart Sven (författare)
Department of Thorac. Clinical Physiology, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden
Wojtaszewski, Jörgen F. P. (författare)
Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA, United States;
Dufresne, Scott D. (författare)
Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA, United States
Horton, Edward S. (författare)
Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA, United States
Ljungqvist, Olle, 1954- (författare)
Örebro universitet,Institutionen för medicinska vetenskaper,Department of Surgery, Huddinge University Hospital, Huddinge, Sweden
Goodyear, Laurie J. (författare)
Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA, United States; Metabolism Section, Joslin Diabetes Center, Boston MA, United States
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 (creator_code:org_t)
American Physiological Society, 1999
1999
Engelska.
Ingår i: American Journal of Physiology. - : American Physiological Society. - 0002-9513 .- 2163-5773. ; 277:4, s. E733-E741
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • 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 translocationphenomenon 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 · min-1). On another day, subjects exercised for 60 min at 70% of maximal oxygen consumption (VO(2max)), 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 inresponse 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.

Ämnesord

MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Physiology (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Fysiologi (hsv//swe)
MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine (hsv//eng)

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