| Project/Area Number |
15K11384
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Periodontology
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| Research Institution | Niigata University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
NAKAMURA KAZUTOSHI 新潟大学, 医歯学系, 教授 (70207869)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2015: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | 歯周炎 / 脱共役タンパク / 閉経後女性 / 遺伝子多型 / 歯周医学 / マクロファージ / 歯周病原細菌 / 骨粗鬆症 / 歯学 / 遺伝子 / 免疫学 |
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| Outline of Final Research Achievements |
Uncoupling proteins (UCPs) are mitochondrial membrane transporters which regulate the metabolism of carbohydrate, lipid, and bone. Genetic polymorphisms in UCPs are risk factors for diabetes, obesity and osteoporosis. Periodontitis has been reported to be associated with the systemic diseases. Therefore, we investigated the associations among UCP polymorphisms, periodontitis, diabetes, obesity and osteoporosis. As a result, UCP2 and UCP3 polymorphisms were associated with severe periodontitis independently of the systemic diseases, though the prevalence of periodontitis was not associated with the polymorphisms. Moreover, to elucidate the biological role of UCP2 in periodontitis, we performed experiments in human macrophages. The suppression of UCP2 expression significantly elevated the levels of reactive oxygen species and proinflammatory cytokines. The results suggested that UCPs may play roles in the pathogenesis of periodontitis.
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