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

SDT 大鼠（自发性糖尿病模型）的血管内皮细胞在体外表现出对 VEGF 的增强反应。对过度信号传导的药理学抑制可抑制 SDT 大鼠的胰腺 b 细胞损失和糖尿病的发展。这些数据提示了糖尿病发生的一个新机制，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损伤胰腺b细胞的分泌因子增加，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.