| Project/Area Number |
24790743
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Circulatory organs internal medicine
|
|---|
| Research Institution | The University of Tokyo |
|---|
Principal Investigator |
ISHIDA Junichi 東京大学, 医学部附属病院, 助教 (10625536)
|
|---|
| Project Period (FY) |
2012-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
|---|
| Keywords | 肥満 / 2型糖尿病 / 小型脂肪細胞 / KLF6 / 糖尿病 / 転写因子KLF6 |
|---|
| Outline of Final Research Achievements |
Obesity and type 2 diabetes are the major risk factors of cardiovascular disease, and it is essential to elucidate the underlying mechanism. Transcription factor KLF6 promotes adipocyte differentiation, and heterozygote KLF6 knockout mice were resistant to high fat-induced obesity and fatty liver. These findings indicate that KLF6 is involved in the pathomechanism of obesity and type 2 diabetes.
Hepatocyte-specific, adipocyte-specific and macrophage-specific KLF6 knockout mice were fed high-fat diet. Hepatocyte-specific and adipocyte-specific KLF6 deletion resulted in suppressed weight gain and reduced hepatic fatty change compared with control group. KLF6 indirectly promoted the expression of PPAR alpha in hepatocyte. These results could also provide a new insight for the treatment of obesity and type 2 diabetes.
|
