Investigation of pathogenesis of NAFLD in disturbance of hepatic and intestinal Toll-like receptor signal and alternation of microbiota
| Project/Area Number |
23790758
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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 |
Gastroenterology
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
SAWADA Koji 旭川医科大学, 大学病院, 特任助教 (80548660)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | NAFLD / Toll-like receptor (TLR) / 脂肪酸 / 前炎症状態 / 腸肝軸 / 非アルコール性脂肪性肝疾患 / toll-like receptor / TLRシグナル |
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| Research Abstract |
In this study, we investigated the expression of TLRs in gut-liver axis in high fat fed mice. The expression of TLRs was already upregulated in NAFLD liver without inflammation, but downregulated in small intestine. Antibiotics treatment improved steatosis and TLR expression in the liver. Fatty acids upregulated TLRs expression in Kupffer cell and hepatocyte models. In the development of the pro-inflammatory state of NAFLD, fatty acids trigger the expressions of TLRs, which contribute to the induction of inflammatory cytokines through TLR signals by the intestinal microbiota.
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Report
(3 results)
Research Products
(14 results)
