Regulation of pancreatic beta cell mass via glucokinase-dependent and independent pathways

GKA刺激的IRS 2产生影响β细胞增殖。氧化应激减弱了GKA对参与β细胞功能和增殖的基因表达变化的影响。GKA能够通过IRS-2依赖性途径和IRS-2非依赖性调节ER应激相关基因的表达来改善ER应激介导的细胞凋亡。胰腺部分切除术是评价啮齿类动物β细胞适应性增殖的良好模型。我们研究了葡萄糖激酶和IRS-2在这些小鼠模型中的作用，并注意到部分胰腺切除术后β细胞增殖既不需要葡萄糖激酶也不需要IRS-2。总的来说，我们研究了通过葡萄糖激酶依赖性和。独立的道路。

GKA-stimulated IRS2 production affected beta cell proliferation. Oxidative stress diminished the effects of GKA on the changes in expression of genes involved in beta cell function and proliferation. GKA was able to ameliorate ER stress-mediated apoptosis via both IRS-2-dependent pathway and IRS-2-independent regulation of the expressions of genes related to ER stress. Partial pancreatectomy is a good model for the evaluation of adaptive proliferation ofβcells in rodents. We investigated the roles of glucokinase and IRS-2 in these mouse models and noted that neither glucokinase nor IRS-2 was required forβcell proliferation after partial pancreatectomy. Collectively, we investigated the regulation of pancreaticβcell mass via glucokinase-dependent and. independent pathways.