| Project/Area Number |
23790362
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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 |
Pathological medical chemistry
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| Research Institution | Mie University |
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Principal Investigator |
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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 |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 代謝異常学 / メタボリックシンドローム / 炎症 / シグナル伝達 / マクロファージ / 生活習慣病 |
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| Research Abstract |
In recent studies, it is revealed that chronic low-grade inflammation is involved in rising insulin resistance and metabolic syndrome. p38 is known as stress-activated protein kinase of mitogen-activated protein kinase (MAPK) family. To investigate the p38α functions in metabolic syndrome, we produced conditional knockout mice of p38α, in which p38α gene was disrupted in hematopoietic cells and vascular endotherial cells.In the p38α conditional knockout (cKO) mice, high fat diet-induced insulin resistance and obesity were significantly suppressed. High fat diet-induced infiltration of macrophage into adipose tissue was also suppressed in the p38α cKO mice. Expression level of genes regulating inflammation and chemotaxis was altered in the adipose tissue and ATM (adipose tissue macrophage) of the p38α cKO mice. These observations indicate that p38α is involved in the high fat diet-induced insulin resistance, probably through modifying macrophage infiltration. Furthermore, the expression of lipid metabolism genes was changed in liver of the p38α cKO mice. It suggests that p38αin blood cells regulates obesity via lipid metabolism in liver.
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