Insulin/adenosine axis linked signalling

Silva, Luis, Subiabre, Mario, Araos, Joaquín, Saez, Tamara, Salsoso, Rocío, Pardo, Fabian, Leiva, Andrea, San Martin, Rody, Toledo, Fernando and Sobrevia, Luis (2016) Insulin/adenosine axis linked signalling. Molecular Aspects of Medicine, 55 45-61. doi:10.1016/j.mam.2016.11.002

Author Silva, Luis
Subiabre, Mario
Araos, Joaquín
Saez, Tamara
Salsoso, Rocío
Pardo, Fabian
Leiva, Andrea
San Martin, Rody
Toledo, Fernando
Sobrevia, Luis
Title Insulin/adenosine axis linked signalling
Journal name Molecular Aspects of Medicine   Check publisher's open access policy
ISSN 1872-9452
Publication date 2016-11-19
Sub-type Article (original research)
DOI 10.1016/j.mam.2016.11.002
Open Access Status Not yet assessed
Volume 55
Start page 45
End page 61
Total pages 17
Place of publication Kidlington, Oxford, United Kingdom
Publisher Pergamon Press
Language eng
Formatted abstract
Regulation of blood flow depends on systemic and local release of vasoactive molecules such as insulin and adenosine. These molecules cause vasodilation by activation of plasma membrane receptors at the vascular endothelium. Adenosine activates at least four subtypes of adenosine receptors (A1AR, A2AAR, A2BAR, A3AR), of which A2AAR and A2BAR activation leads to increased cAMP level, generation of nitric oxide, and relaxation of the underlying smooth muscle cell layer. Vasodilation caused by adenosine also depends on plasma membrane hyperpolarization due to either activation of intermediate-conductance Ca2+-activated K+ channels in vascular smooth muscle or activation of ATP-activated K+ channels in the endothelium. Adenosine also causes vasoconstriction via a mechanism involving A1AR activation resulting in lower cAMP level and increased thromboxane release. Insulin has also a dual effect causing NO-dependent vasodilation, but also sympathetic activity- and increased endothelin 1 release-dependent vasoconstriction. Interestingly, insulin effects require or are increased by activation or inactivation of adenosine receptors. This is phenomenon described for d-glucose and l-arginine transport where A2AAR and A2BAR play a major role. Other studies show that A1AR activation could reduce insulin release from pancreatic β-cells. Whether adenosine modulation of insulin biological effect is a phenomenon that depends on co-localization of adenosine receptors and insulin receptors, and adenosine plasma membrane transporters is something still unclear. This review summarizes findings addressing potential involvement of adenosine receptors to modulate insulin effect via insulin receptors with emphasis in the human vasculature.
Keyword Adenosine
Smooth muscle
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: UQ Centre for Clinical Research Publications
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