2014 Fiscal Year Final Research Report
Molecular mechanism for pancreatic beta-cell glucose toxicity
| Project/Area Number |
24591327
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Metabolomics
|
|---|
| Research Institution | Kawasaki Medical School (2013-2014)
Osaka University (2012) |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
MATSUOKA Taka-aki 大阪大学, 医学系研究科, 講師 (10379258)
MIYATSUKA Takeshi 大阪大学, 医学系研究科, 講師 (60622363)
|
|---|
| Project Period (FY) |
2012-04-01 – 2015-03-31
|
| Keywords | 膵β細胞機能 |
|---|
| Outline of Final Research Achievements |
It is well known that pancreatic transcription factor PDX-1 plays a crucial role in maintenance of pancreatic beta-cell function but that its expression level is decreased under diabetic conditions. We made beta-cell-specific PDX-1 overexpressing transgenic mice. As the results, such PDX-1 overexpresion ameliorated glycemic control in diabetic Akita mice.
It is also known that incretins (GLP-1 and GIP) play a crucial role in maintenance of beta-cell function but that GLP-1 and GIP receptor levels are decreased. We made beta-cell-specific GLP-1 receptor overexpressing transgenic mice. As the results, such GLP-1 receptor overexpresion augmented exendin-4-mediated insulin secretion in diabetic db/db mice.
|
| Free Research Field |
糖尿病
|
