| Project/Area Number |
20590941
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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 |
Kidney internal medicine
|
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| Research Institution | Tohoku University |
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Principal Investigator |
NAKAYAMA Masaaki Tohoku University, 医学部, 教授 (60217940)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SATO Toshinobu 東北大学, 病院, 准教授 (50312583)
|
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| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2010: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2009: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2008: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 腎臓学 / 慢性腎臓病 / メタボリック症候群 / 生活習慣病 / 糖代謝産物 / メチルグリオキサール / ギ酸 |
|---|
| Research Abstract |
Chronic kidney disease (CKD) and life-style related metabolic disorders such as hypertension, and diabetes, are independent risk factors for excess cardiovascular events, however the common pathological mechanisms or causative molecules have remained to be addressed. The present study identified glucose degraded molecule ? methylglyoxal as one of the candidates. Methylglyoxal induces cellular and organ damage by enhancing oxidative stress. Furthermore, it was suggested that the degraded process of methylglyoxal may facilitate purine metabolism, leading to uric acid production.
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