2012 Fiscal Year Final Research Report
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 |
Research Field |
Gastroenterology
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Research Institution | Asahikawa Medical College |
Principal Investigator |
SAWADA Koji 旭川医科大学, 大学病院, 特任助教 (80548660)
|
Project Period (FY) |
2011 – 2012
|
Keywords | NAFLD / Toll-like receptor (TLR) / 脂肪酸 / 前炎症状態 / 腸肝軸 |
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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Research Products
(5 results)