异丙肾上腺素对胰岛素释放的双重作用在下丘脑肥胖大鼠的胰岛中受到抑制。
The dual effect of isoproterenol on insulin release is suppressed in pancreatic islets from hypothalamic obese rats.
作者信息
Marçal Anderson Carlos, Grassiolli Sabrina, da Rocha Diego Neves, Puzzi Marcelo Aguilar, Gravena Clarice, Scomparin Dionízia Xavier, de Freitas Mathias Paulo Cezar
机构信息
Laboratory of Secretion Cell Biology, Department of Cell Biology and Genetics, State University of Maringá, Maringá, PR, Brazil.
出版信息
Endocrine. 2006 Jun;29(3):445-9. doi: 10.1385/endo:29:3:445.
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.
肥胖中的高胰岛素血症被认为是胰腺β细胞胰岛素分泌过多所致。β细胞配备有胆碱能和肾上腺素能受体；虽然总的乙酰胆碱作用是增强作用，但儿茶酚胺的作用是通过α2肾上腺素能受体抑制葡萄糖诱导的胰岛素释放（GIIR）。然而，已表明β肾上腺素能激动剂可增强葡萄糖反应。对通过L-谷氨酸单钠（MSG）新生儿期处理获得的高胰岛素血症成年肥胖大鼠的胰岛中的GIIR进行了研究。MSG大鼠的胰岛对葡萄糖的反应性比对照大鼠更高。β肾上腺素能激动剂异丙肾上腺素抑制了MSG肥胖大鼠胰岛中的GIIR。结果表明，MSG处理导致β细胞肾上腺素能受体功能发生改变。
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