The study on the effect that a reduction of insulin-sensitive hormone causes periodontal disease in diabetes patients

胰岛素敏感激素减少对糖尿病患者牙周病影响的研究

基本信息

批准号：
17592184
负责人：
YAMAGUCHI Noboru
金额：
$ 2.18万
依托单位：
KYUSHU UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2005
资助国家：
日本
起止时间：
2005 至 2006
项目状态：
已结题

项目摘要

Our previous epidemiologic studies suggested that periodontal disease is closely related to obesity and glucose tolerance. Since the level of adiponectin, an adipocyte-derived cytokine, in plasma had been reported to decrease in obese and type 2 diabetes patients, we explored the role of adiponectin in the etiology of periodontitis by using the D clone of RAW 264, which clone exhibits highly efficient osteoclast formation, to determine whether adiponectin acts as a regulatory molecule in osteoclast formation stimulated by lipopolysaccharide (LPS) of periodontopathic bacteria.We observed that adiponectin acted as a potent inhibitor of osteoclast formation stimulated by Toll-like receptor 4 (TLR4) ligand and receptor activator of NF-κB ligand (RANKL). Since NF-κB is an important transcriptional factor in osteoclast formation, we examined the effect of the adiponectin on its transcriptional activity. Our luciferase assay showed that adiponectin was able to inhibit the TLR4-mediated NF-κB activity in RAW 264 cells. In addition, we observed that the cytokine was actually able to inhibit TLR4-mediated expression of the gene for inducible nitric oxide synthase and production of nitric oxide in the cells. These observations strongly suggest that adiponectin may function as a negative regulator of LPS/RANKL-mediated osteoclast formation in periodontal disease.

我们以前的流行病学研究表明，牙周疾病与肥胖和葡萄糖耐受密切相关。 Since the level of adiponectin, an adipocyte-derived cytokine, in plasma had been reported to decrease in obese and type 2 diabetes patients, we explored the role of adiponectin in the etiology of periodontitis by using the D clone of RAW 264, which clone exhibits highly efficient osteoclast formation, to determine whether adiponectin acts as a regulatory molecule in牙周病细菌的脂多糖（LPS）刺激的破骨细胞形成。我们观察到，脂联素充当了由Toll-like受体4（TLR4）配体和受体激活剂NF-κB-bigand（cankl）刺激的破骨细胞形成的潜在抑制剂。由于NF-κB是破骨细胞形成的重要转录因子，因此我们检查了脂联素对其转录活性的影响。我们的荧光素酶测定法表明脂联素能够抑制RAW 264细胞中TLR4介导的NF-κB活性。此外，我们观察到，细胞因子实际上能够抑制该基因对诱导型一氧化氮合酶的TLR4介导的表达和细胞中一氧化氮的产生。这些观察结果强烈表明脂联素可能是牙周疾病中LPS/RANKL介导的破骨细胞形成的负调节剂。

项目成果

期刊论文数量（16）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Adiponectin inhibits Toll-like receptor family-induced signaling

DOI：
10.1016/j.febslet.2005.11.019
发表时间：
2005-12-19
期刊：
FEBS LETTERS
影响因子：
3.5
作者：
Yamaguchi, N;Guillermo, J;Yamashita, Y
通讯作者：
Yamashita, Y

ヒト血漿レプチン濃度と甘味感受性との相関

人血浆瘦素浓度与甜味敏感性的相关性

DOI：
发表时间：
2006
期刊：
日本味と匂学会誌 12
影响因子：
0
作者：
中村由紀;太田理恵;山口登;城崎慎也;山下喜久;古谷野潔;野中和明;重村憲徳;ニノ宮裕三
通讯作者：
ニノ宮裕三

Adiponectin inhibits osteoclast formation stimulated by lipopolysaccharide from Actinobacillus actinomycetemcomitans.

DOI：
10.1111/j.1574-695x.2006.00164.x
发表时间：
2007-02
期刊：
FEMS immunology and medical microbiology
影响因子：
0
作者：
N. Yamaguchi;T. Kukita;Yin-Ji Li;Jose Guillermo Martinez Argueta;Toshiyuki Saito;S. Hanazawa;Y. Yamashita
通讯作者：
N. Yamaguchi;T. Kukita;Yin-Ji Li;Jose Guillermo Martinez Argueta;Toshiyuki Saito;S. Hanazawa;Y. Yamashita

糖尿病患者における口腔内ケアの重要性

糖尿病患者口腔护理的重要性