| Project/Area Number |
21590918
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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 |
Circulatory organs internal medicine
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| Research Institution | Department of Clinical Research, National Hospital Organization Kyoto Medical Center |
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Principal Investigator |
WADA Hiromichi 独立行政法人国立病院機構(京都医療センター臨床研究センター), 展開医療研究部, 研究室長(先端医療技術開発) (20416209)
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| Co-Investigator(Kenkyū-buntansha) |
SATOH Noriko 独立行政法人国立病院機構(京都医療センター臨床研究センター), 糖尿病研究部, 研究室長(臨床代謝栄養) (80373512)
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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 | メタボリックシンドローム / 喫煙 / バイオマーカー / 肥満 / 脂質異常 / 動脈硬化 / 血管新生 / リンパ管新生 / トランスレーショナルリサーチ / 循環器・高血圧 / 細胞・組織 / 動物 / 臨床 / トランスレーションリサーチ |
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| Research Abstract |
The mechanisms that lead from obesity to atherosclerotic disease are not fully understood. Obesity involves angiogenesis in which vascular endothelial growth factor-A(VEGF-A) plays a key role. Soluble VEGF receptor-2(sVEGFR-2) acts as an endogenous inhibitor of VEGF-A. We demonstrated that serum levels of sVEGFR-2 are increased in sera from subjects with metabolic syndrome in association with insulin resistance. We also showed that the sVEGFR-2 level, as well as the body mass index, significantly increases after successful smoking cessation. A recent study reported that sVEGFR-2 also acts as an endogenous inhibitor of vascular endothelial growth factor-C(VEGF-C). We found that VEGF-C, rather than VEGF-A, is closely related to dyslipidemia and atherosclerosis.
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