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  • Title: The dual effect of isoproterenol on insulin release is suppressed in pancreatic islets from hypothalamic obese rats.
    Author: Marçal AC, Grassiolli S, da Rocha DN, Puzzi MA, Gravena C, Scomparin DX, de Freitas Mathias PC.
    Journal: Endocrine; 2006 Jun; 29(3):445-9. PubMed ID: 16943583.
    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 glucose-induced insulin release (GIIR) via alpha2-adrenoceptor. However, it has been shown that beta-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 beta-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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