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

Research Project

Project/Area Number	21790378
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Single-year Grants
Research Field	Experimental pathology
Research Institution	Chiba University
Principal Investigator	KAWAMURA Harukjyo Chiba University, 大学院・医学研究院, 助教 (70527902)
Co-Investigator(Renkei-kenkyūsha)	IWANAGA Toshihiko 北海道大学, 組織細胞学分野, 教授 (10160128)
Project Period (FY)	2009 – 2010
Project Status	Completed (Fiscal Year 2010)
Budget Amount *help	¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000) Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000) Fiscal Year 2009: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Keywords	糖尿病 / sDTラット / VEGF / 血管内皮細胞 / SDTラット
Research Abstract	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.