Elucidating the mechanism by which hepatic steatosis induces inflammation and insulin resistance
| Project/Area Number |
20790489
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Kanazawa University |
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Principal Investigator |
KURITA Seiichiro Kanazawa University, 医学系, 協力研究員 (20436819)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2008: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | インスリン抵抗性 / 肝臓 / 脂肪化 / 炎症 / ミトコンドリア / 酸化ストレス / 脂肪細胞 / タンパク分解系 / 骨格筋 / プロテアソーム |
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| Research Abstract |
We have shown that inflammation and insulin resistance (IR) accelerates nonalcoholic fatty liver disease. This study examined the mechanism by which hepatic steatosis induces inflammation and IR. When we treated hepatocytes (rat H4IIEC3 cells) with fatty acid (palmitate), JNK was activated via mitochondria-derived reactive oxygen species. Since JNK induces inflammation and apoptosis, this result tied inflammation to hepatic steatosis. In addition, we showed that obesity caused dysfunction of the hepatic protein resolution system, and enhanced this gene cluster to compensate for this. The dysfunction of the protein resolution system induced hepatic IR. In the future, I hope to clarify this mechanism and develop new treatments for nonalcoholic fatty liver disease and hepatitis C, which are exacerbated by IR and hepatic steatosis, and metabolic syndrome and type 2 diabetes mellitus, which are systemic conditions related to IR.
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Report
(3 results)
Research Products
(2 results)
