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Exercise signalling to glucose transport in skeletal muscle

Published online by Cambridge University Press:  05 March 2007

Erik A. Richter*
Affiliation:
Copenhagen Muscle Research Centre, Department of Human Physiology, Institute of Exercise and Sport Sciences, University of Copenhagen, Universitetsparken 13, 2100, Copenhagen Ø, Denmark
Jakob N. Nielsen
Affiliation:
Copenhagen Muscle Research Centre, Department of Human Physiology, Institute of Exercise and Sport Sciences, University of Copenhagen, Universitetsparken 13, 2100, Copenhagen Ø, Denmark
Sebastian B. Jørgensen
Affiliation:
Copenhagen Muscle Research Centre, Department of Human Physiology, Institute of Exercise and Sport Sciences, University of Copenhagen, Universitetsparken 13, 2100, Copenhagen Ø, Denmark
Christian Frøsig
Affiliation:
Copenhagen Muscle Research Centre, Department of Human Physiology, Institute of Exercise and Sport Sciences, University of Copenhagen, Universitetsparken 13, 2100, Copenhagen Ø, Denmark
Jesper B. Birk
Affiliation:
Copenhagen Muscle Research Centre, Department of Human Physiology, Institute of Exercise and Sport Sciences, University of Copenhagen, Universitetsparken 13, 2100, Copenhagen Ø, Denmark
Jørgen F. P. Wojtaszewski
Affiliation:
Copenhagen Muscle Research Centre, Department of Human Physiology, Institute of Exercise and Sport Sciences, University of Copenhagen, Universitetsparken 13, 2100, Copenhagen Ø, Denmark
*
*Corresponding author: Dr Erik A. Richter Fax: +45 35 32 16 00, Email: [email protected]
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Abstract

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Contraction-induced glucose uptake in skeletal muscle is mediated by an insulin-independent mechanism that leads to translocation of the GLUT4 glucose transporter to the muscle surface membrane from an intracellular storage site. Although the signalling events that increase glucose transport in response to muscle contraction are not fully elucidated, the aim of the present review is to briefly present the current understanding of the molecular signalling mechanisms involved. Glucose uptake may be regulated by Ca2+-sensitive contraction-related mechanisms, possibly involving Ca2+/calmodulin-dependent protein kinase II and some isoforms of protein kinase C. In addition, glucose transport may be regulated by mechanisms that reflect the metabolic status of the muscle, probably involving the 5′AMP-activated protein kinase. Furthermore, the p38 mitogen-activated protein kinase may be involved in activating the GLUT4 translocated to the surface membrane. Nevertheless, the picture is incomplete, and fibre type differences also seem to be involved.

Type
Symposium 1: Exercise signalling pathways controlling fuel oxidation during and after exercise
Copyright
Copyright © The Nutrition Society 2004

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