Department of Medical cell Biology, Uppsala University, Uppsala, Sweden.
Horm Metab Res. 2013 Mar;45(3):252-4. doi: 10.1055/s-0032-1323843. Epub 2012 Sep 26.
Overexpression of α2A-adrenoceptors contributes to type 2 diabetes in GK rats. We aimed to investigate if α2-adrenoceptor inhibition affected islet blood flow in these rats. Anesthetized GK and Wistar-F rats were given the α2-adrenoceptor inhibitor yohimbine (2.5 mg/kg BW) intravenously. The GK rats had higher blood glucose and serum insulin concentrations than WF rats. Yohimbine affected neither of these values in WF rats, but decreased blood glucose and increased serum insulin concentrations in GK rats. Total pancreatic and islet blood flows, measured with microspheres, were increased in GK when compared to WF rats. Yohimbine affected none of the blood flow values in WF rats, whereas islet blood flow in GK rats was reduced to values similar to those seen in WF rats. Overexpression of α2-adrenoceptors may contribute to the increased islet blood flow seen in GK rats, and may be eligible for pharmacologic intervention.
α2A-肾上腺素受体的过度表达导致 GK 大鼠发生 2 型糖尿病。本研究旨在探讨 α2-肾上腺素受体抑制是否会影响这些大鼠胰岛的血流。麻醉的 GK 和 Wistar-F 大鼠静脉给予 α2-肾上腺素受体抑制剂育亨宾（2.5mg/kgBW）。与 Wistar-F 大鼠相比，GK 大鼠的血糖和血清胰岛素浓度更高。育亨宾对 Wistar-F 大鼠的这些值均没有影响，但降低了 GK 大鼠的血糖并增加了其血清胰岛素浓度。用微球测量的总胰腺和胰岛血流在 GK 大鼠中高于 Wistar-F 大鼠。育亨宾对 Wistar-F 大鼠的任何血流值均没有影响，而 GK 大鼠的胰岛血流减少至与 Wistar-F 大鼠相似的水平。α2A-肾上腺素受体的过度表达可能导致 GK 大鼠中胰岛血流增加，并且可能适合进行药物干预。
Zotero 插件