Development of a method for preventing NASH progression and hepatocarcinogenesis by using butyrate-produding probiotics
| Project/Area Number |
23590755
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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 |
Hygiene
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| Research Institution | Tokai University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 予防医学 / 肝発癌予防 / 肝線維化予防 / プロバイオティクス / 酪酸 / NAFLD/NASH / 酪酸菌 / 肝線維化 / 肝発癌 / NASH / Nrf2 / CDAA食 / 脂質過酸化 / エンドトキシン |
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| Research Abstract |
We used a CDAA diet to establish rat NASH model. Rats treated with CDAA diet containing 10% MIYAIRI588, a pharmaceutical product of C. butyricum, reduced CDAA-diet induced hepatic lipid deposition and significantly improved the triglyceride content, insulin resistance, serum endotoxin levels, and hepatic inflammatory indexes. We also found that MIYAIRI 588 substantially increased the activation of hepatic AMPK and AKT and Nrf2 and its targeted antioxidative enzymes, which suppressed hepatic oxidative stress. In vitro studies revealed that sodium butyrate (NaB) activated AMPK and AKT and enhanced Nrf2 expression. NaB-mediated AMPK activation induced the phosphorylation and nuclear translocation of Sirtuin 1, leading to the increased assembly of mTOR complex 2 and phosphorylation of AKT and subsequent induction of Nrf2 expression and activation. These data clearly showed that the butyrate-producing probiotic MIYIRI 588 has beneficial effects in the prevention of NASH progression.
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Report
(4 results)
Research Products
(19 results)
