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activator GW505516 has no acute effect on glucose transport in skeletal muscle
1 Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA
* To whom correspondence should be addressed. E-mail: jhollosz{at}im.wustl.edu.
It has been reported that treatment of cultured human skeletal muscle myotubes with the peroxisome proliferator-activated receptor 
(PPAR) activator GW501516 directly stimulates glucose transport and enhances insulin action. Cultured myotubes are minimally responsive to insulin stimulation of glucose transport and are not a good model for studying skeletal muscle glucose transport. The purpose of this study was to evaluate the effect of GW501516 on glucose transport in order to determine if the findings on cultured myotubes have relevance to skeletal muscle. Rat epitrochlearis and soleus muscles were treated for 6h with either 10 nM, 100 nM or 500 nM GW501516, followed by measurement of 2-deoxyglucose uptake. GW501516 had no effect on glucose uptake. There was no effect on insulin sensitivity or responsiveness. Also in contrast to findings on myotubes, treatment of muscles with GW501516 did not result in increased phosphorylation or increased expression of AMP-activated protein kinase or p38 mitogen activated protein kinase. Treatment of epitrochlearis muscles with GW501516 for 24h induced a 3-fold increase in uncoupling protein 3 (UCP3) mRNA, providing evidence that the GW501516 compound that we used gets into and is active in skeletal muscle. In conclusion, our results show that, in contrast to myotubes in culture, skeletal muscle does not respond to GW501516 with a) an increase in AMPK or p38 MAPK phosphorylation or expression, or b) direct stimulation of glucose transport or enhanced insulin action.
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