| Project/Area Number |
23791038
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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 |
Metabolomics
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| Research Institution | Kumamoto University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
MATSUMURA Takeshi 熊本大学, 大学院・生命科学研究部, 助教 (20398192)
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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 |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | メタボリックシンドローム / 単球 / マクロファージ / 糖尿病 / マクロファージ増殖 / 動脈硬化 / 炎症性サイトカイン |
|---|
| Research Abstract |
In this study we investigate the implication of monocyte/macrophage inflammation andproliferation in diabetes progression. Macrophage and monocyte cultured in high glucoseshowed activated inflammatory activity, and pulsate stimulation with high glucose inducedsignificantly increased inflammatory cytokine expression. Along with the increase ofinflammatory activity, the cell cycle inhibitor, p27kip expression was increased, andmacrophage proliferation was inhibited in high glucose culture. On the other hand, themacrophage specific p27kip transgenic mouse, whose macrophage proliferation is inhibited,showed improved glucose tolerance after high fat diet loading. Further studies arenecessary to reveal the pathophysiological roles of monocyte/macrophage inflammation andproliferation in the progression of diabetes.
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