| Project/Area Number |
10557103
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B).
|
| Allocation Type | Single-year Grants |
|---|
| Section | 展開研究 |
|---|
| Research Field |
Metabolomics
|
|---|
| Research Institution | INSTITUTE FOR MOLECULAR AND CELLULAR RBGULTION (I.M.C.R.), GUNMA UNIVERSITY |
|---|
Principal Investigator |
TAMEMOTO Hiroyuki I.M.C.R.GUNMA UNIV, ERSITY Department of Molecular Medicine Assistant Professor, 生体調節研究所, 講師 (90292630)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
IZUMI Tetsuro I.M.C.R.GUNMA UNIV, ERSITY Department of Molecular Medicine Professor, 生体調節研究所, 教授 (00212952)
|
|---|
| Project Period (FY) |
1998 – 2000
|
| Project Status |
Completed (Fiscal Year 2000)
|
| Budget Amount *help |
¥9,800,000 (Direct Cost: ¥9,800,000)
Fiscal Year 2000: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1999: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1998: ¥5,900,000 (Direct Cost: ¥5,900,000)
|
|---|
| Keywords | insulin resistance / PPARg / knockout mouse / PPARγ / チアゾリジンジオン |
|---|
| Research Abstract |
We made knockout mice of the peroxysomal proliferator activated receptor (PPAR γ) which is the receptor for the insulin sensitizer, thiazolidinedione. The homozygous fetus died in the uterus and we could not make a library from homozygous adult mice. The fibroblasts taken from the homozygous fetus were refractory to induction of the development to the adipocyte. The heterozygous mice were apparently healthy and were relatively resistant to obesity when fed high fat diet as compared with the wild type. They also showed better insulin sensitivity after high fat diet (Kubota N.et al. 1999) The homozygous fetus died between 10 to 11 days after coitus and showed no gross anatomical abnormality. The placenta of the homozygous fetus was impaired in the development of its labyrinth zone. We made a negative dominant construct of PPARγ (Pro427Leu) and subcloned this cDNA in a vector that express the gene under control of Cre-loxP system. We are planning to express the negative dominant PPAR in a tissue specific manner.
|
