| Project/Area Number |
16H07067
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Periodontology
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| Research Institution | Kyushu University |
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Principal Investigator |
SANO TOMOMI 九州大学, 歯学研究院, 助教 (50782075)
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| Project Period (FY) |
2016-08-26 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 炎症 / エピカテキン / 脂肪組織 / 歯周組織 / 肥満 / インスリン抵抗性 / 慢性炎症 / 抗炎症 / 脂肪細胞 / マクロファージ / 歯周炎 / 歯周病 / ケモカイン |
|---|
| Outline of Final Research Achievements |
Epicatechin (EC) suppressed the expression of many inflammatory genes in the adipocytes co-cultured with endotoxin-stimulated macrophages. Specifically, EC markedly suppressed chemokine (C-C motif) ligand 19 (CCL19) expression. The in vivo study indicated that mice fed the EC-supplemented HFD were protected from diet-induced obesity and insulin resistance. The expression levels of genes associated with inflammation in adipose tissue and in the liver were downregulated in this group of mice.
EC exerts beneficial effects for the prevention of adipose tissue inflammation and insulin resistance. Since the mice deficient in the CCL19 receptor were protected from diet-induced obesity and insulin resistance, the beneficial effects of EC could be mediated, at least in part, by marked suppression of CCL19 expression. Thus, EC may also exert beneficial effects against periodontal inflammation-associated augmentation of cardiovascular risk.
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