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This Article Full Text Full Text (PDF) All Versions of this Article: 297/4/E924    most recent 90653.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Maarbjerg, S. J. Articles by Richter, E. A. PubMed PubMed Citation Articles by Maarbjerg, S. J. Articles by Richter, E. A.

Genetic impairment of AMPK2 signaling does not reduce muscle glucose uptake during treadmill exercise in mice

¹Department of Exercise and Sport Sciences, Section of Human Physiology, Molecular Physiology Group and Copenhagen Muscle Research Centre; and ²Institute of Sports Medicine, Bispebjerg Hospital and Center for Healthy Aging, Faculty of Health Sciences, Copenhagen Muscle Research Centre, University of Copenhagen, Copenhagen, Denmark

Submitted 5 August 2008 ; accepted in final form 14 July 2009

Some studies suggest that the 5'-AMP-activated protein kinase (AMPK) is important in regulating muscle glucose uptake in response to intense electrically stimulated contractions. However, it is unknown whether AMPK regulates muscle glucose uptake during in vivo exercise. We studied this in male and female mice overexpressing kinase-dead AMPK2 (AMPK-KD) in skeletal and heart muscles. Wild-type and AMPK-KD mice were exercised at the same absolute intensity and the same relative intensity (30 and 70% of individual maximal running speed) to correct for reduced exercise capacity of the AMPK-KD mouse. Muscle glucose clearance was measured using 2-deoxy-[³H]glucose as tracer. In wild-type mice, glucose clearance was increased at 30 and 70% of maximal running speed by 40 and 350% in the quadriceps muscle and by 120 and 380% in gastrocnemius muscle, respectively. Glucose clearance was not lower in AMPK-KD muscles compared with wild-type regardless of whether animals were exercised at the same relative or the same absolute intensity. In agreement, surface membrane content of the glucose transporter GLUT4 was increased similarly in AMPK-KD and wild-type muscle in response to running. We also measured signaling of alternative exercise-sensitive pathways that might be compensatorily increased in AMPK-KD muscles. However, increases in phosphorylation of CaMKII, Trisk95, p38 MAPK, and ERK1/2 were not higher in AMPK-KD than in WT muscle. Collectively, these findings suggest that AMPK2 signaling is not essential in regulating glucose uptake in mouse skeletal muscle during treadmill exercise and that other mechanisms play a central role.

adenosine 5'-monophosphate-activated protein kinase; glucose transport; molecular signaling