| Project/Area Number |
17590947
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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 | Saitama Medical University |
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Principal Investigator |
INOUE Ikuo Saitama Medical University, Faculty of Medicine, Associated professor, 医学部, 助教授 (60232526)
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| Co-Investigator(Kenkyū-buntansha) |
IKEDA Masaaki Saitama Medical University, Faculty of Medicine, Associated professor, 医学部, 助教授 (80232198)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | PPARalpha / PPARdelta / beta / PPARgamma / BMAL1 / CLOCK / RORalpha / RORbeta / REV-ERB / PPARγ / ROR / PPARδ / BNAL1 / CRBPII |
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| Research Abstract |
Lipid absorption and metabolism are regulated by feeding and by the circadian system. It has been suggested that the expression of enzymes involved in lipid metabolism is directly controlled by the clock system. This study was designed to examine whether or not the promoter activities of peroxisome proliferator-activated receptor (PPAR) has transcriptional activity via the CLOCK/BMAL1 heterodimer. Male mice 8-12 weeks old were maintained under a 12 : 12 hour light-dark cycle for at least two weeks before the day of the experiment. The mRNA profiles of BMAL1 and of the PPAR were measured in intestine. The direct effects of CLOCK/BMAL1 on the promoter activities of PPAR were assessed in vitro by luciferase assay. The expression of PPAR target genes changed in a cyclical manner that followed expression of BMAL1. The promoter activities of the PPAR were increased by CLOCK/BMAL1 expression. After deletion of the promoter of PPAR, CLOCK/BMAL1 did not affect transactivation. PPAR transactivates.
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