PMID: 9549052Apr 29, 1998Paper

Decreased insulin content and secretion in RIN 1046-38 cells overexpressing alpha 2-adrenergic receptors

Endocrine
M S Rodriguez-PenaA M Spiegel

Abstract

Several Gi-protein-coupled receptors normally expressed in islet beta-cells inhibit insulin secretion on binding of their respective agonists. To study the effect of supraphysiologic expression of such a receptor in insulin-secreting beta-cells, we stably transfected cDNA encoding the mouse alpha 2a-adrenergic receptor into RIN 1046-38 cells. Four different cell lines were selected, each overexpressing the alpha 2a-adrenergic receptor to varying degrees. Cell lines showing the highest level of receptor expression showed significantly reduced insulin content, and reduced basal and stimulated insulin secretion. Pertussis toxin (PTX) treatment of cells was able to reverse partially the reduced insulin secretory response. Our results suggest that overexpression of a Gi-protein-coupled receptor in beta-cells causes tonic inhibition of both insulin synthesis and secretion. Abnormalities in expression or function of such receptors could be a contributory factor in the impaired insulin secretion present in type II diabetes.

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Citations

Feb 13, 2002·Drug Discovery Today·Alan WiseStephen Rees
Apr 12, 2012·American Journal of Physiology. Cell Physiology·Susanne G Straub, Geoffrey W G Sharp
May 1, 2015·Archives of Endocrinology and Metabolism·Marciane WelterFabiane Gomes de Moraes Rego
Sep 15, 2005·The Journal of Biological Chemistry·Michelle E KimplePatrick J Casey

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