| Project/Area Number |
25862043
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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 |
Periodontology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
Mizutani Koji 東京医科歯科大学, 医歯(薬)学総合研究科, 助教 (60451910)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 歯周病 / 肥満 / インスリン抵抗性 / 糖尿病 / 歯周炎 |
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| Outline of Final Research Achievements |
Gingival samples were collected from fatty (ZF) and lean (ZL, control) Zucker rats. Activities of protein kinase C (PKC) were significantly increased in the gingiva from ZF rats compared with those from ZL rats. Expression of oxidative stress markers was significantly increased in ZF rats. Analysis of the gingiva showed that insulin-induced phosphorylation of IRS-1, Akt, and eNOS was significantly decreased in ZF rats, but Erk1/2 activation was not affected. General PKC inhibitor and an anti-oxidant normalized the action of insulin on Akt and eNOS activation in the gingiva from ZF rats. This provided the first documentation of obesity-induced insulin resistance in the gingiva. Analysis of our data suggested that PKC activation and oxidative stress may selectively inhibit insulin-induced Akt and eNOS activation, causing endothelial dysfunction and inflammation.
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