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Diabetes 55:3588-3593, 2006
DOI: 10.2337/db06-0555
© 2006 by the American Diabetes Association
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Reduced Expression of Gi in Erythrocytes of Humans With Type 2 Diabetes Is Associated With Impairment of Both cAMP Generation and ATP Release

Randy S. Sprague, Alan H. Stephenson, Elizabeth A. Bowles, Madelyn S. Stumpf, and Andrew J. Lonigro

From the Department of Pharmacological and Physiological Science, Saint Louis University, School of Medicine, St. Louis, Missouri

Address correspondence and reprint requests to Randy S. Sprague, Saint Louis University, School of Medicine, Department of Pharmacological and Physiological Science, 1402 South Grand Blvd., St. Louis, MO 63104. E-mail: spraguer{at}slu.edu

Abbreviations: AC, adenylyl cyclase; IBMX, 3-isobutyl-1-methyl xanthine; PVDF, polyvinylidene difluoride

Human erythrocytes, by virtue of their ability to release ATP in response to physiological stimuli, have been proposed to participate in the regulation of local blood flow. A signal transduction pathway that relates these stimuli to ATP release has been described and includes the heterotrimeric G protein Gi and adenylyl cyclase (AC). In this cell, Gi activation results in increases in cAMP and, ultimately, ATP release. It has been reported that Gi expression is decreased in animal models of diabetes and in platelets of humans with type 2 diabetes. Here, we report that Gi2 expression is selectively decreased in erythrocytes of humans with type 2 diabetes and that this defect is associated with reductions in cAMP accumulation and ATP release in response to incubation of erythrocytes with mastoparan 7 (10 µmol/l), an activator of Gi. Importantly, this defect in ATP release correlates inversely with the adequacy of glycemic control as determined by levels of HbA1c (A1C). These results demonstrate that in erythrocytes of humans with type 2 diabetes, both Gi expression and ATP release in response to mastoparan 7 are impaired, which is consistent with the hypothesis that this defect in erythrocyte physiology could contribute to the vascular disease associated with this clinical condition.


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Copyright © 2006 by the American Diabetes Association.