| Project/Area Number |
04671457
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
内分泌・代謝学
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| Research Institution | University of Tsukuba |
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Principal Investigator |
OKUDA Yukichi Inst. of Clin. Med., University of Tsukuba Associate professor, 臨床医学系・内科, 助教授 (60211132)
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| Project Period (FY) |
1992 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1994: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1993: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1992: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | Diabetic Angiopathy / Vascular endothelial cell / Aortic Smooth muscle cell / High glucose / Myo-inositol / Eicosapentaenoic acid / PDGF / Nitric oxide / 糖尿病 / 血管障害 / Angiotensin II / アルドース還元酵素阻害剤 |
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| Research Abstract |
Hyperglycemia is believed to be the major cause of diabetic vascular complications. We evaluated the effect of high glucose on polyol mechanism, PDGF production in human umbilical vein endothelial cells (HUE) and aortic smooth muscle cell (ASMC). (1) Myo-inositol incorporation into endothelial cells may be dependent on an active transport system via Na^+-K^+-ATPase activity. (2) Eicosapentaenoic acid (EPA) and Aldose-reductase inhibitor (ONO 2235) decreased glucose mediated inhibition of myo-inositol uptake. (3) Under excess of ambient glucose (13.8,27.5 mM) and a hyperosmolar condition (122.0 mOsm/L with mannitol), PDGF in culture medium were both significantly incresed. Parallel to protein secretion levels, PDGF-B chain mRNA levels showed a significant increase. (4) EPA enhanced NO production in HUE.Also EPA inhibited migration of ASMC induced by PDGF.(5) After administration of EPA,Lipo PGE_1, the blood flow of the lower extremity of diabetic patients significantly increased.
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