increased vascular permeabi I ity contributes to the development of diabetes in SDT rats

自发性糖尿病模型SDT大鼠血管内皮细胞对VEGF的反应增强。药理学抑制过度信号传导抑制胰腺B细胞损失和发展的糖尿病在SDT大鼠。这些数据提示了糖尿病发展的新机制，即胰腺B细胞分泌的VEGF诱导胰腺血管内皮细胞过度信号传导，导致血管功能障碍或分泌因子增加损伤胰腺B细胞，导致胰腺B细胞死亡。

Vascular endothelial cells of SDT rat, a spontaneously diabetic model, showed enhanced response against VEGF in vitro. Pharmacological inhibition of the excessive signaling suppressed pancreatic b cell loss and development of diabetes in SDT rats. These data suggests a new mechanism of diabetes development that VEGF secreted from pancreatic b cells induces excessive signaling in pancreatic vascular endothelial cells, which causes vascular dysfunction or increase in secretion factors injuring pancreatic b cells, leading to the pancreatic b cell death.