The dual effect of isoproterenol on insulin release is suppressed in pancreatic islets from hypothalamic obese rats |
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| Authors: | Marçal Anderson Carlos Grassiolli Sabrina da Rocha Diego Neves Puzzi Marcelo Aguilar Gravena Clarice Scomparin Dionízia Xavier de Freitas Mathias Paulo Cezar |
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| Affiliation: | (1) Laboratory of Secretion Cell Biology, Department of Cell Biology and Genetics, State University of Maringá, Av Colombo, 5790, 87020-900 Maringá, PR, Brazil |
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| Abstract: | Hyperinsulinemia in obesity has been attributed to insulin oversecretion by pancreatic beta-cells. Beta-cells are equipped with cholinergic and adrenergic receptors; whereas overall acetylcholine action is to potentiate, catecholamines' effect is to inhibit glucoseinduced insulin release (GIIR) via α2-adrenoreceptor. However, it has been shown that -adrenergic agonists potentiate glucose response. GIIR was studied in pancreatic islets from hyperinsulinemic adult obese rats, obtained by l-glutamate monosodium (MSG) neonatal treatment. Islets from MSG-rats were more glucose responsive than control ones. Isoproterenol, a -adrenergic agonist, inhibited the GIIR in islets from MSG-obese rats. Results indicate that MSG treatment causes alteration on function of beta-cell adrenoceptors. |
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| Keywords: | -Adrenergic receptors insulin secretion MSG-obesity pancreatic islets |
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