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内皮胰岛素抵抗恶化实验性牙周炎

T Zeze¹, T Shinjo¹, K Sato¹

¹Section of Periodontology, Faculty of Dental Science, Kyushu University, Fukuoka, Japan.

Journal of dental research

|July 14, 2023

概括

牙内皮胰岛素抵抗通过增加VCAM1表达和白细胞粘附来促进牙周炎. 这通过减少PI3K/Akt/FoxO1通路激活而发生,恶化气泡骨损失.

科学领域:

口腔生物学口腔生物学
内分泌学在内分泌学.
免疫学免疫学免疫学

背景情况:

在糖尿病患者中,牙周炎的严重程度更高.
与糖尿病相关的牙周炎的分子机制尚不清楚.
牙组织中的胰岛素抵抗可能会导致糖尿病并发症.

研究的目的:

调查牙周炎病原发生过程中牙的作用中的内皮胰岛素耐药性.
阐明将内皮胰岛素抵抗与牙周炎联系起来的分子机制.

主要方法:

通过PI3K/Akt途径检查了胰岛素对内皮细胞 (ECs) 中VCAM1表达的作用.
使用了血管内皮细胞特异性胰岛素受体淘汰 (VEIRKO) 的小鼠.
分析了FoxO1在胰岛素介导的VCAM1调节和白细胞粘附中的作用.

主要成果:

胰岛素治疗通过PI3K/Akt降低了EC中的VCAM1表达,减少了白细胞粘附.
超血糖引起的胰岛素抵抗在ECs减少了胰岛素对VCAM1.1的影响.
在VEIRKO小鼠中,牙周炎和骨质损失增加,VCAM1,TNFα,MCP-1和RANKL的上调.
在VEIRKO小鼠和经过高血糖治疗的EC中,胰岛素介导的FoxO1激活被抑制.
突变的FoxO1减弱了胰岛素对VCAM1和白细胞粘附的调节.

结论:

内皮胰岛素抵抗有助于牙周炎的进展.
失调的VCAM1表达和白细胞粘附是PI3K/Akt/FoxO1信号受损的结果.
向内皮胰岛素抵抗可能为糖尿病患者的牙周炎提供治疗策略.

关键词:

这是一个VCAM-1系统.气泡骨损失是指气泡骨损失的发生.细胞粘附分子的细胞粘附分子甲盒蛋白质O1 是一种甲盒蛋白质.牙周疾病牙周疾病 2 型糖尿病 2 型糖尿病

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