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Am J Physiol Endocrinol Metab (March 30, 2004). doi:10.1152/ajpendo.00082.2004
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Submitted on February 20, 2004
Accepted on December 31, 1969

Phorbol Esters Affect Skeletal Muscle Glucose Transport in a Fiber Type Specific Manner

David C. Wright1, Paige C. Geiger1, Mark J. Rheinheimer1, Dong Ho Han1, and John O. Holloszy1*

1 Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA

* To whom correspondence should be addressed. E-mail: jhollosz{at}im.wustl.edu.

Recent evidence has shown that activation of lipid sensitive protein kinase C (PKC) isoforms leads to skeletal muscle insulin resistance. However, earlier studies demonstrated that phorbol esters increase glucose transport in skeletal muscle. The purpose of the present study was to try to resolve this discrepancy. Treatment with the phorbol ester, dPPA, led to a ~3.5 fold increase in glucose transport in isolated fast twitch epitrochlearis and FDB muscles. Phorbol ester treatment was additive to a maximally effective concentration of insulin in fast twitch skeletal muscles. Treatment with dPPA did not affect insulin signaling in the epitrochlearis. In contrast, phorbol esters had no effect on basal glucose transport, and inhibited maximally insulin stimulated glucose transport ~50%, in isolated slow twitch soleus muscle. Furthermore, dPPA treatment inhibited the insulin stimulated tyrosine phosphorylation of IRS-1 and the threonine and serine phosphorylation of PKB by ~50% in the soleus. dPPA treatment also caused serine phosphorylation of IRS-1 in the slow twitch soleus muscle. In conclusion, our results show that phorbol esters stimulate glucose transport in fast twitch skeletal muscles and inhibit insulin signaling in slow twitch soleus muscle of rats. These findings suggest that mechanisms other than PKC activation mediate lipotoxicity induced whole body insulin resistance.




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