Exercise and insulin cause GLUT-4 translocation in human skeletal muscle

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Standard

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 tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Thorell, A, Hirshman, MF, Nygren, J, Jorfeldt, L, Wojtaszewski, J, Dufresne, SD, Horton, ES, Ljungqvist, O & Goodyear, LJ 1999, 'Exercise and insulin cause GLUT-4 translocation in human skeletal muscle', American Journal of Physiology - Endocrinology and Metabolism, bind 277, nr. 4 (40-4), s. E733-E741. https://doi.org/10.1152/ajpendo.1999.277.4.E733

APA

Thorell, A., Hirshman, M. F., Nygren, J., Jorfeldt, L., Wojtaszewski, J., Dufresne, S. D., Horton, E. S., Ljungqvist, O., & Goodyear, L. J. (1999). Exercise and insulin cause GLUT-4 translocation in human skeletal muscle. American Journal of Physiology - Endocrinology and Metabolism, 277(4 (40-4)), E733-E741. https://doi.org/10.1152/ajpendo.1999.277.4.E733

Vancouver

Thorell A, Hirshman MF, Nygren J, Jorfeldt L, Wojtaszewski J, Dufresne SD o.a. Exercise and insulin cause GLUT-4 translocation in human skeletal muscle. American Journal of Physiology - Endocrinology and Metabolism. 1999;277(4 (40-4)):E733-E741. https://doi.org/10.1152/ajpendo.1999.277.4.E733

Author

Thorell, Anders ; Hirshman, Michael F ; Nygren, Jonas ; Jorfeldt, Lennart ; Wojtaszewski, Jørgen ; Dufresne, Scott D ; Horton, Edward S ; Ljungqvist, Olle ; Goodyear, Laurie J. / Exercise and insulin cause GLUT-4 translocation in human skeletal muscle. I: American Journal of Physiology - Endocrinology and Metabolism. 1999 ; Bind 277, Nr. 4 (40-4). s. E733-E741.

Bibtex

@article{dd2e130a00aa403c96bde063fdbc9140,
title = "Exercise and insulin cause GLUT-4 translocation in human skeletal muscle",
abstract = "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.",
keywords = "Akt, Glucose disposal, Glucose transporters, Glucose uptake, Muscle contraction",
author = "Anders Thorell and Hirshman, {Michael F} and Jonas Nygren and Lennart Jorfeldt and J{\o}rgen Wojtaszewski and Dufresne, {Scott D} and Horton, {Edward S} and Olle Ljungqvist and Goodyear, {Laurie J}",
note = "(Ekstern)",
year = "1999",
doi = "10.1152/ajpendo.1999.277.4.E733",
language = "English",
volume = "277",
pages = "E733--E741",
journal = "A J P: Endocrinology and Metabolism (Online)",
issn = "1522-1555",
publisher = "American Physiological Society",
number = "4 (40-4)",

}

RIS

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