Project/Area Number |
19209034
|
Research Category |
Grant-in-Aid for Scientific Research (A)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Metabolomics
|
Research Institution | Tohoku University |
Principal Investigator |
OKA Yoshitomo Tohoku University, 大学院・医学系研究科, 教授 (70175256)
|
Co-Investigator(Kenkyū-buntansha) |
石原 寿光 東北大学, 病院, 講師 (60361086)
石垣 泰 東北大学, 病院, 助教 (50375002)
山田 哲也 東北大学, 病院, 助教 (90400374)
|
Co-Investigator(Renkei-kenkyūsha) |
ISHIHARA Hisamitsu 日本大学, 医学部・内科学系, 教授 (60361086)
YAMADA Tetsuya 東北大学, 大学院・医学系研究科, 准教授 (90400374)
ISHIGAKI Yasusi 東方大学, 病院, 講師 (50375002)
|
Project Period (FY) |
2007 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥49,660,000 (Direct Cost: ¥38,200,000、Indirect Cost: ¥11,460,000)
Fiscal Year 2009: ¥14,430,000 (Direct Cost: ¥11,100,000、Indirect Cost: ¥3,330,000)
Fiscal Year 2008: ¥14,430,000 (Direct Cost: ¥11,100,000、Indirect Cost: ¥3,330,000)
Fiscal Year 2007: ¥20,800,000 (Direct Cost: ¥16,000,000、Indirect Cost: ¥4,800,000)
|
Keywords | インスリン分泌 / 膵β細胞 / 小胞体ストレス / 再生治療 / 増殖 |
Research Abstract |
Pancreatic β cell mass contributes to the development of diabetes. We show that induction of 4E-BP1 promotes β cell survival under ER stress. The Eif4ebp1 gene encoding 4E-BP1 was revealed to be a direct target of the transcription factor ATF4. We also found that hepatic activation of extracellular regulated kinase signaling induced pancreatic β cell proliferation through a neuronal-mediated relay of metabolic signals. Thus, inter-organ metabolic relay systems may serve as valuable targets in regenerative treatments for diabetes.
|