| Project/Area Number |
25461014
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Aichi Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
Ito Kiyoaki 愛知医科大学, 肝胆膵内科, 教授 (50551420)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | ストレス / 交感神経系 / ＮＡＳＨ / ＮＡＦＬＤ / 脂肪性肝炎 / 脂肪肝 / ＣＰＴ１ / NASH / 交感神経 / 肥満 / 糖尿病 / 高脂肪食 / CRF / 非アルコール性脂肪性肝炎 / ノルアドレナリン / フェニレフリン / イソプロテレノル / ＣＲＦ |
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| Outline of Final Research Achievements |
To investigate the effect of sympathetic nervous system which is activated by stress on NASH, alpha-adrenergic receptor agonist, phenylephrine and beta-adrenergic receptor agonist, isoproterenol were administered to mice concurrent with high fat diet feeding. Four weeks after the commencement of feeding, hepatic histological findings were evaluated. While hepatic steatosis was not changed by phenylephrine, isoproterenol augmented hepatic steatosis. Microarray and Real time PCR showed that hepatic CPT1 mRNA level, which is related to beta-oxidation in mitocondria tended to be decreased in isoproterenol-treated mice. These indicates that beta-adrenergic agonist stimulates hepatic steatosis through the suppression of beta-oxidation in NASH.
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