Exercise and insulin cause GLUT-4 translocation in human skeletal muscle
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Exercise and insulin cause GLUT-4 translocation in human skeletal muscle. / Thorell, Anders; Hirshman, Michael F; Nygren, Jonas; Jorfeldt, Lennart; Wojtaszewski, Jørgen; Dufresne, Scott D; Horton, Edward S; Ljungqvist, Olle; Goodyear, Laurie J.
I: American Journal of Physiology - Endocrinology and Metabolism, Bind 277, Nr. 4 (40-4), 1999, s. E733-E741.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Exercise and insulin cause GLUT-4 translocation in human skeletal muscle
AU - Thorell, Anders
AU - Hirshman, Michael F
AU - Nygren, Jonas
AU - Jorfeldt, Lennart
AU - Wojtaszewski, Jørgen
AU - Dufresne, Scott D
AU - Horton, Edward S
AU - Ljungqvist, Olle
AU - Goodyear, Laurie J
N1 - (Ekstern)
PY - 1999
Y1 - 1999
N2 - 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 · 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 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.
AB - 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 · 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 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.
KW - Akt
KW - Glucose disposal
KW - Glucose transporters
KW - Glucose uptake
KW - Muscle contraction
UR - http://www.scopus.com/inward/record.url?scp=0032758457&partnerID=8YFLogxK
U2 - 10.1152/ajpendo.1999.277.4.E733
DO - 10.1152/ajpendo.1999.277.4.E733
M3 - Journal article
C2 - 10516134
AN - SCOPUS:0032758457
VL - 277
SP - E733-E741
JO - A J P: Endocrinology and Metabolism (Online)
JF - A J P: Endocrinology and Metabolism (Online)
SN - 1522-1555
IS - 4 (40-4)
ER -
ID: 242716969