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Am J Physiol Endocrinol Metab (September 23, 2008). doi:10.1152/ajpendo.90362.2008
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Submitted on April 14, 2008
Revised on September 22, 2008
Accepted on September 22, 2008

The {alpha} subunit of AMPK is essential for submaximal contraction-mediated glucose transport in skeletal muscle in vitro {alpha}

Natalie Simard-Lefort1, Emmanuelle St-Amand1, Sebastien Morasse1, Claude H. Cote2, and Andre Marette3*

1 Laval University Hospital Research Center
2 CHUL Research Center
3 Centre hospitalier de l'Universite Laval

* To whom correspondence should be addressed. E-mail: andre.marette{at}crchul.ulaval.ca.

AMPK is a key signaling pathway in the regulation of skeletal muscle glucose uptake but its role in mediating contraction-induced glucose transport is still debated. The effect of contraction on glucose transport is impaired in EDL muscle of transgenic mice expressing a kinase-dead, dominant negative form of the AMPK {alpha}2 subunit (KD-{alpha}2AMPK mice). However, maximal force production is reduced in this muscle, raising the possibility that the defect in glucose transport was due to a secondary decrease in force production and not impaired AMPK {alpha}2 activity. Generating force : frequency curves revealed that muscle force production is matched between wild-type (WT) and KD-{alpha}2AMPK mice at frequencies ≤ 50 Hz. Moreover, AMPK activation is already maximal at 50 Hz in muscles of WT mice. When EDL muscles from WT mice were stimulated at a frequency of 50 Hz for 2 min (200ms train, 1/s, 30V), contraction caused a ~3.5-fold activation of AMPK{alpha}2 activity and a ~2-fold stimulation of glucose uptake. Conversely, while force production was similar in EDL of KD-{alpha}2AMPK animals, no effect of contraction was observed on AMPK{alpha}2 activity and glucose uptake stimulation was reduced by 50% (P<0.01) As expected, AICAR caused a 2.3-fold stimulation of AMPK{alpha}2 activity and a 1.7-fold increase in glucose uptake in EDL from wild-type (WT) mice while no effect was detected in muscle from KD-{alpha}2AMPK mice. These data demonstrate that AMPK activation is essential for both AICAR and submaximal contraction-induced glucose transport in skeletal muscle, but that AMPK-independent mechanisms are also involved.




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