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1 Division of Geriatrics and Nutritional Sciences, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA
* To whom correspondence should be addressed. E-mail: dhan{at}im.wustl.edu.
Increases in contraction stimulated glucose transport in fast twitch rat epitrochlearis muscle is mediated by AMPK and Ca2+/CAMK dependent signaling pathways. However, recent studies provide evidence suggesting that contraction stimulated glucose transport in slow twitch skeletal muscle is mediated through an AMPK independent pathway. The purpose of the present study was to test the hypothesis that contraction stimulated glucose transport in rat slow twitch soleus muscle is mediated by an AMPK independent/Ca2+ dependent pathway. Caffeine, an SR Ca2+ releasing agent, at a concentration that does not cause muscle contractions or decreases in high energy phosphates, led to an ~ 2 fold increase in 2-DG uptake in isolated split soleus muscles. This increase in glucose transport was prevented by the SR calcium channel blocker dantrolene and the CAMK inhibitor, KN93. Conversely, AICAR, an AMPK activator had no effect on 2-DG uptake in isolated split soleus muscles yet resulted in an ~ 2 fold increase in the phosphorylation of AMPK and its downstream substrate, acetyl coA carboxylase. The hypoxia induced increase in 2-DG uptake was prevented by dantrolene and KN93, while hypoxia stimulated phosphorylation of AMPK was unaltered by these agents. Tetanic muscle contractions resulted in a ~ 3.5 fold increase in 2-DG uptake that was prevented by KN93, which did not prevent AMPK phosphorylation. Taken in concert, our results provide evidence that hypoxia and contraction stimulated glucose transport is mediated entirely through a Ca2+dependent mechanism in rat slow twitch muscle.
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