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26. Activation of the A1 adenosine receptor increases insulin-stimulated glucose transport in isolated rat soleus muscle.

Author

Lally, Jamie S.V., Dyck, David J., Greer, Felicia, Bonen, Arend, Graham, Terry E., and Thong, Farah S.L.

Subjects
GLUCOSE, MUSCLE contraction, ADENOSINE deaminase, BIOLOGICAL transport, WESTERN immunoblotting, PROTEINS
Abstract

Copyright of Applied Physiology, Nutrition & Metabolism is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2007
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30. Activation of the A1 adenosine receptor increases insulin-stimulated glucose transport in isolated rat soleus muscle.

Author

Thong FS, Lally JS, Dyck DJ, Greer F, Bonen A, and Graham TE

Subjects
3-O-Methylglucose metabolism, Adenosine administration & dosage, Adenosine analogs & derivatives, Adenosine pharmacology, Adenosine A1 Receptor Antagonists, Animals, Biological Transport drug effects, Biological Transport physiology, Cell Membrane metabolism, Dose-Response Relationship, Drug, Glucose Transporter Type 4 metabolism, In Vitro Techniques, Male, RNA, Messenger metabolism, Rats, Rats, Wistar, Receptor, Adenosine A1 genetics, Receptor, Adenosine A1 metabolism, Xanthines administration & dosage, Xanthines pharmacology, Adenosine physiology, Glucose metabolism, Insulin pharmacology, Muscle, Skeletal metabolism, Receptor, Adenosine A1 physiology
Abstract

The A1 adenosine receptor (A1AR) has been suggested to participate in insulin- and contraction-stimulated glucose transport in skeletal muscle, but the qualitative and quantitative nature of the effect are controversial. We sought to determine if A1AR is expressed in rat soleus muscle and then characterize its role in glucose transport in this muscle. A1AR mRNA and protein expression were determined by RT-PCR and Western blotting, respectively. To examine the role of adenosine in 3-O-methylglucose transport, isolated muscles were exposed to adenosine deaminase and alpha,beta-methylene adenosine diphosphate to remove endogenous adenosine and were left unstimulated (basal) or stimulated with insulin. To assess the functional participation of A1AR in 3-O-methylglucose transport, muscles were incubated with A1-selective agonist and (or) antagonist in the absence of endogenous adenosine and with or without insulin. A1AR mRNA was expressed in soleus muscle and A1AR was present at the plasma membrane. Removal of endogenous adenosine reduced glucose transport in response to 100 microU/mL insulin (approximately 50%). The A1-selective agonist, N6-cyclopentyladenosine, increased submaximal (100 microU/mL) insulin-stimulated glucose transport in a dose-dependent manner (0.001-1.0 micromol/L). This stimulatory effect was inhibited by the A1-selective receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine in a concentration-dependent manner (0.001-1.0 micromol/L). However, neither activation nor inhibition of A1AR altered basal or maximal (10 mU/mL) insulin-stimulated glucose transport. Our results suggest that adenosine contributes approximately 50% to insulin-stimulated muscle glucose transport by activating the A1AR. This effect is limited to increasing insulin sensitivity, but not to either basal or maximal insulin-stimulated glucose uptake in rat soleus muscle.

Published
2007
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