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Glucose decreases extracellular adenosine levels in isolated mouse and rat pancreatic islets

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Yang, G. K., Squires, Paul E., Tian, Faming, Kieffer, T. J., Kwok, Y. N. and Dale, Nicholas (2012) Glucose decreases extracellular adenosine levels in isolated mouse and rat pancreatic islets. Islets, Vol.4 (No.1). doi:10.4161/isl.4.1.19037

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Abstract

The pancreatic islets of Langerhans are responsible for the regulated release of the endocrine hormones insulin and glucagon that participate in the control of glucose homeostasis. Abnormal regulation of these hormones can result in glucose intolerance and lead to the development of diabetes. Numerous efforts have been made to better understand the physiological regulators of insulin and glucagon secretion. One of these regulators is the purine nucleoside, adenosine. Though exogenous application of adenosine has been demonstrated to stimulate glucagon release and inhibit insulin release, the physiological significance of this pathway has been unclear. We used a novel 7 µm enzyme-coated electrode biosensor to measure adenosine levels in isolated rodent islets. In the mouse islets, basal adenosine levels in the presence of 3 mM glucose were estimated to be 5.7 ± 0.6 µM. As glucose was increased, extracellular adenosine diminished. A 10-fold increase of extracellular KCl increased adenosine levels to 16.4 ± 2.0 µM. This release required extracellular Ca2+ suggesting that it occurred via an exocytosis-dependent mechanism. We also found that while rat islets were able to convert exogenous ATP into adenosine, mouse islets were unable to do this. Our study demonstrates for the first time the basal levels of adenosine and its inverse relationship to extracellular glucose in pancreatic islets.

Item Type: Journal Article
Subjects: Q Science > Q Science (General)
Divisions: Faculty of Science > Life Sciences (2010- )
Journal or Publication Title: Islets
Publisher: Landes Bioscience
ISSN: 1938-2014
Official Date: January 2012
Dates:
DateEvent
January 2012Published
Volume: Vol.4
Number: No.1
DOI: 10.4161/isl.4.1.19037
Status: Peer Reviewed
Publication Status: Published
Access rights to Published version: Restricted or Subscription Access

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