| Project/Area Number |
10671066
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | Osaka University |
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Principal Investigator |
KASAYAMA Soji Osaka University Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (10240839)
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| Co-Investigator(Kenkyū-buntansha) |
SAITO Hiroshi Osaka University Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (90301259)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 1999: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1998: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | adipocyte / C / EBP / PPAR-γ / knockout mouse / thiazolidinedione / SCD-1 / molecular biology / GLUT-4 / LPL / EBP-β / EBP-δ / インスリン抵抗性 |
|---|
| Research Abstract |
It is shown that C/EBP family proteins and PPAR-γ play important roles on adipocyte differentiation. However, the precise roles of each molecule have not been defined. To explore this issue, we transfected C/EBP-β and -δ double knockout mouse embryonic fibroblasts with adenovirus vector containing mouse PPAR-γ2 (pAdex-mPPARγ2). When the pAdex-mPPARγ2-transfected cells were stimulated with troglitazone or 15-deoxy-△ィイD112.14ィエD1-PGJ2, they became to show mature adipocyte phenotype stained with oil-red-O. Intracellular triglyceride content and SCD-1 and aP2 mRNA levels of these cells did not differ, compared with wild-type mouse embryonic fibroblasts transfected with pAdex-mPPARγ2. However, LPL and GLUT4 mRNA levels were significantly lower in these cells. Thus, forced expression of PPAR-γ2 alone can induce adipocyte differentiation in the absence of C/EBP-β and C/EBP-γ, although C/EBP-β and /or C/EBP-δ are important for the expression of some adipocyte-specific genes.
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