| Project/Area Number |
21591140
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | The University of Tokushima |
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Principal Investigator |
AIHARA Ken-ichi 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 講師 (70372711)
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| Co-Investigator(Kenkyū-buntansha) |
AKAIKE Masashi 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 教授 (90271080)
IWASE Takashi 徳島大学, 病院, 助教 (10403718)
ENDOU Itsurou 徳島大学, 病院, 講師 (10432759)
HUJINAKA Yuichi 徳島大学, 病院, 講師 (30432751)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ヘパリンコファクターII / トロンビン / 心筋リモデリング / インスリン抵抗性 / メタボリックシンドローム / 2型糖尿病 |
|---|
| Research Abstract |
We hypothesized that thrombin inactivation ameliorate cardiac remodeling and diabetes. Angiotensin II accelerated cardiac concentric remodeling and larger left atrial volume with prominent interstitial fibrosis in heparin cofactor II(HCII), an endogenous thrombin inhibitor,-deficient mice than those in wild-type mice. And these cardiac phenotypes were caused by enhancement of NAD(P) H oxidase-transforming growth factor-beta1 pathway. In addition, we found that increased thrombin activity in adipose tissue contributes to the development of insulin resistance via enhancing MCP-1 production, leading to macrophage infiltration and insulin receptor substrate-1-Akt pathway inactivation.
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