Stöckli Jacqueline, James David E
Garvan Institute of Medical Research, 384 Victoria St., Darlinghurst, NSW, Australia.
Cell Metab. 2009 Mar;9(3):213-4. doi: 10.1016/j.cmet.2009.02.005.
Insulin signaling is key to the etiology of metabolic syndrome. Recent work (Luan et al., 2009) uncovers a role for beta-arrestin, previously known to control GPCR desensitization, in insulin signaling. In mouse models, beta-arrestin-2 controls whole-body insulin action by regulating assembly of a complex containing insulin receptor, c-Src, and Akt.
胰岛素信号传导是代谢综合征病因的关键。最近的研究（Luan等人，2009年）揭示了β-抑制蛋白在胰岛素信号传导中的作用，β-抑制蛋白此前已知可控制G蛋白偶联受体（GPCR）的脱敏。在小鼠模型中，β-抑制蛋白2通过调节包含胰岛素受体、c-Src和Akt的复合物的组装来控制全身胰岛素作用。
