| Project/Area Number |
24700776
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Applied health science
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| Research Institution | National Cardiovascular Center Research Institute |
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Principal Investigator |
WENG Huachun 独立行政法人国立循環器病研究センター, 研究所, 非常勤研究員 (80598053)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | ペルオキシソーム / 脂肪肝 / 脂肪酸 / 代謝 / 肝臓 / 脂肪酸代謝 / 中性脂肪蓄積 / 増殖 / 脂肪酸酸化 / 脂質蓄積 / 非アルコール性脂肪肝 |
|---|
| Research Abstract |
Peroxisomes have many important functions in lipid metabolism, including fatty acid beta-oxidation. Pex11a is a Pex gene factor required for peroxisome biogenesis. To examine the functions of the Pex11a gene, we disrupted this gene in mice. Pex11a knock out (KO) mice showed significantly higher body weights and hepatic triglyceride (TG) concentrations than wild type (WT) mice fed a normal diet or a high-fat diet. Hepatic TG in fasted KO mice was significantly higher than those in fasted WT mice. KO mice exhibited fewer irregular and functional peroxisomes than WT mice. Fenofibrate increased peroxisome abundance and decreased body weight. mRNA levels of peroxisomal fatty acid oxidation-related genes were significantly higher in WT mice than KO mice. Our results demonstrated that Pex11a in involved in peroxisome proliferation and fatty acid beta-oxidation, and activation of Pex11a and/or the peroxisomes might be an excellent therapeutic strategy against non-alcohol fatty liver.
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