| Project/Area Number |
11671086
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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 |
Endocrinology
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| Research Institution | Osaka University |
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Principal Investigator |
NAKAMURA Tadashi Osaka University Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (90252668)
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| Co-Investigator(Kenkyū-buntansha) |
KIHARA Shinji Osaka University Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手
FUNAHASHI Tohru Osaka University Graduate School of Medicine, Lecturer, 医学系研究科, 講師 (60243234)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2000: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1999: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | adiponectin / obesity / type 2 diabetes / atherosclerosis / vascular endothelial cell / adohesion molecule / TNF-α / NFκB / 脂肪細胞 / 冠動脈疾患 / 糖尿病 |
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| Research Abstract |
We identified a novel adipocyte-derived matrix protein, adiponectin, which is abundantly present in the circulation. We showed that obese subjects and subjects with coroary artery disease (CAD) exhibited decreased plasma concentrations of adiponectin and also, in vitro study, that this protein suppressed the attachment of monocytes to endothelial cells through the decreased expression of adhesion molecules such as ICAM-1, VCAM-1, and E-selectin, which is an early event in atherosclerotic vascular change.
In the present study, we observed the relationship between plasma adiponectin concentrations and disorders susceptible to atherosclerosis including type 2 diabetes, and aiso clarified the molecular mechanism in its anti-atherogenic actions.
We confirmed that plasma adiponectin cncentrations were decreased in many obese subjects and the subjects with CAD.Furthermore, we observed plasma levels of adiponectin in the diabetic subjects without CAD were lower than those in age- and BMI-matched non-diabetic subjects. The plasma adiponectin concentrations of diabetic patients with CAD were lower than those of diabetic patients without CAD.Weight reduction significantly elevated plasma adiponectin levels in both the diabetic and the non-diabetic subjects.
We previously observed that adiponectin inhibited tumor necrosis factor-α (TNF-α)-induced expression of endothelial adhesion molecules. In the current study, we demonstrated that adiponectin specifically supressed TNF-α-induced IκB-α-NFκB activation through a cAMP -dependent pathway in human aortic endothelial cells.
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