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牙周炎和牙周洁治对肥胖大鼠胰岛素抵抗和肝组织 CD36 的影响。

Influence of periodontitis and scaling and root planing on insulin resistance and hepatic CD36 in obese rats.

机构信息

Department of Periodontics, Stomatological Hospital of Southern Medical University, Guangdong Provincial Stomatological Hospital, Guangzhou, 510280, China.

Vice President, Savaid Medical School of University of Chinese Academy of Sciences, Beijing, 100049, China.

出版信息

J Periodontol. 2018 Apr;89(4):476-485. doi: 10.1002/JPER.17-0115. Epub 2018 Mar 30.

Abstract

BACKGROUND

The aim of the study was to explore the influence of periodontitis and scaling and root planing (SRP) on insulin resistance and hepatic CD36 in obese rats with periodontitis.

METHODS

Thirty-two specific pathogen free Sprague-Dawley rats were randomly divided into four groups of eight animals each as follows: healthy rats (healthy group), obese rats (obesity group), obese rats with periodontitis (non-therapy group), and obese rats with periodontitis who underwent periodontal SRP (therapy group). Rats were fed with a high-fat diet for 16 weeks to build an obesity model. Periodontal inflammation was induced by performing periodontal ligation with Porphyromonas gingivalis. The tissue around the maxillary second molars, bilaterally, were collected. The periodontal attachment level (from the cemento-enamel junction to the bottom of the periodontal pocket) of the second molars was measured in all groups. All rats were subjected to fasting blood glucose, insulin, and serum C-reactive protein tests (CRP). Insulin resistance was evaluated by homeostasis model assessment of insulin resistance (HOMA-IR), oral glucose tolerance test (OGTT), and area under the curve (AUC). The liver was excised to detect intrahepatic free fatty acid (FFA) levels and pathologic observation. Real-time quantification PCR, western blot, and immunohistochemistry were applied to detect hepatic CD36 expression.

RESULTS

Compared with the obesity group, HOMA-IR, AUC, intrahepatic FFA, and protein expression, and mRNA levels of hepatic CD36 in the non-therapy group were significantly increased (P < 0.05). HOMA-IR, AUC, CRP, protein expression, and mRNA levels of hepatic CD36 were all significantly decreased (P < 0.05) 2-weeks after SRP.

CONCLUSIONS

Periodontitis increases insulin resistance while scaling and root planning could improve insulin resistance. Hepatic CD36 regulation may be considered a potential mechanism for this phenomenon.

摘要

背景

本研究旨在探讨牙周炎和牙周刮治(SRP)对伴牙周炎肥胖大鼠胰岛素抵抗和肝 CD36 的影响。

方法

32 只无特定病原体的 Sprague-Dawley 大鼠随机分为 4 组,每组 8 只,分别为:健康大鼠(健康组)、肥胖大鼠(肥胖组)、伴牙周炎的肥胖大鼠(未治疗组)和伴牙周炎并接受牙周 SRP 的肥胖大鼠(治疗组)。大鼠给予高脂饮食喂养 16 周建立肥胖模型。通过用牙龈卟啉单胞菌结扎牙周建立牙周炎炎症。双侧上颌第二磨牙周围组织被收集。所有组均测量第二磨牙的牙周附着水平(从釉牙骨质界到牙周袋底部)。所有大鼠进行空腹血糖、胰岛素和血清 C 反应蛋白(CRP)检测。通过稳态模型评估的胰岛素抵抗(HOMA-IR)、口服葡萄糖耐量试验(OGTT)和曲线下面积(AUC)评估胰岛素抵抗。切除肝脏以检测肝内游离脂肪酸(FFA)水平和病理观察。应用实时定量 PCR、western blot 和免疫组化检测肝 CD36 表达。

结果

与肥胖组相比,未治疗组的 HOMA-IR、AUC、肝内 FFA 以及肝 CD36 的蛋白表达和 mRNA 水平显著增加(P<0.05)。SRP 治疗 2 周后,HOMA-IR、AUC、CRP、肝 CD36 的蛋白表达和 mRNA 水平均显著降低(P<0.05)。

结论

牙周炎会增加胰岛素抵抗,而牙周刮治可以改善胰岛素抵抗。肝 CD36 的调节可能是这种现象的潜在机制。

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