Journal of Applied Physiology AJP: Endocrinology and Metabolism
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J Appl Physiol (August 2, 2002). doi:10.1152/japplphysiol.00445.2002
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Articles in PresS, published online ahead of print August 2, 2002
J Appl Physiol, 10.1152/jap.00445.2002
Submitted on May 17, 2002
Accepted on July 29, 2002

Epinephrine inhibits insulin-stimulated muscle glucose transport

Desmond G Hunt1 and John L Ivy1*

1 Kinesiology and Health Education, University of Texas, Austin, Texas, USA

* To whom correspondence should be addressed. E-mail: johnivy{at}mail.utexas.edu.

We recently demonstrated that epinephrine could inhibit the activation by insulin of IRS-1 associated PI 3-kinase (IRS-1/PI 3-kinase) in skeletal muscle (J. Appl. Physiol. 92: 1285-1292, 2002). Activation of PI 3-kinase is recognized as an essential step in the activation of muscle glucose transport by insulin. We therefore investigated the effect of epinephrine on insulin-stimulated glucose transport in both fast-twitch (epitrochlearis) and slow twitch (soleus) muscle of the rat using an isolated muscle preparation. Glucose transport was significantly increased in the epitrochlearis and soleus when incubated in 50 and 100 µU/ml insulin. Activation of glucose transport by 50 µU/ml insulin was inhibited by 24 nM epinephrine in both muscle types. This inhibition of glucose transport by epinephrine was accompanied by suppression of IRS-1/PI 3-kinase activation. However, when muscles were incubated in 100 µU/ml insulin, 24 nM epinephrine was unable to inhibit IRS-1/PI 3-kinase activation or glucose transport. Even when the epinephrine concentration was increased to 500 nM, no attenuating effect was observed on glucose transport. Results of this study indicate that epinephrine is capable of inhibiting glucose transport activated by a moderate, but not a high physiological insulin concentration. The inhibition of glucose transport by epinephrine appears to involve the inhibition of IRS-1/PI 3kinase activation.




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