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. 2006 Jun;29(3):445-9.
doi: 10.1385/endo:29:3:445.

The dual effect of isoproterenol on insulin release is suppressed in pancreatic islets from hypothalamic obese rats

Anderson Carlos Marçal  1 , Sabrina Grassiolli, Diego Neves da Rocha, Marcelo Aguilar Puzzi, Clarice Gravena, Dionízia Xavier Scomparin, Paulo Cezar de Freitas Mathias
Affiliations

The dual effect of isoproterenol on insulin release is suppressed in pancreatic islets from hypothalamic obese rats

Anderson Carlos Marçal et al. Endocrine. 2006 Jun.

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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