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2 型糖尿病大鼠正畸牙齿移动时腺苷一磷酸激活蛋白激酶活性的起始。

The onset of adenosine monophosphate-activated protein kinase activity on orthodontic tooth movement in rats with type 2 diabetes.

机构信息

State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, China.

出版信息

Eur J Oral Sci. 2023 Oct-Nov;131(5-6):e12955. doi: 10.1111/eos.12955. Epub 2023 Oct 7.

DOI:10.1111/eos.12955
PMID:37805702
Abstract

Adenosine monophosphate-activated protein kinase (AMPK) plays pivotal roles in metabolic diseases including type 2 diabetes. However, the specific role of AMPK for orthodontic tooth movement in type 2 diabetes is unclear. In this study, a diabetic rat model was established through dietary manipulation and streptozocin injection. Examinations were conducted to select qualified type 2 diabetic rats. Then, an orthodontic device was applied to these rats for 0, 3, 7, or 14 days. The distance of orthodontic tooth movement and parameters of alveolar bone were analyzed by micro-computed tomography. Periodontal osteoclastic activity, inflammatory status, and AMPK activity were measured via histological analyses. Next, we repeated the establishment of diabetic rats to investigate whether change of AMPK activity was associated with orthodontic tooth movement under type 2 diabetes. The results showed that diabetic rats exhibited an exacerbated alveolar bone resorption, overactive inflammation, and decreased periodontal AMPK activity during orthodontic tooth movement. Injection of the AMPK agonist alleviated type 2 diabetes-induced periodontal inflammation and alveolar bone resorption, thus normalizing distance of orthodontic tooth movement. Our study indicates that type 2 diabetes decreases periodontal AMPK activity, leading to excessive inflammation elevating osteoclast formation and alveolar bone resorption, which could be reversed by AMPK activation.

摘要

腺苷单磷酸激活蛋白激酶(AMPK)在包括 2 型糖尿病在内的代谢性疾病中发挥着关键作用。然而,AMPK 在 2 型糖尿病正畸牙齿移动中的具体作用尚不清楚。在这项研究中,通过饮食操作和链脲佐菌素注射建立了 2 型糖尿病大鼠模型。进行了检查以选择合格的 2 型糖尿病大鼠。然后,在这些大鼠上应用正畸装置 0、3、7 或 14 天。通过微计算机断层扫描分析正畸牙移动的距离和牙槽骨参数。通过组织学分析测量牙周破骨细胞活性、炎症状态和 AMPK 活性。接下来,我们重复建立糖尿病大鼠以研究在 2 型糖尿病下 AMPK 活性的变化是否与正畸牙移动有关。结果表明,在正畸牙移动过程中,糖尿病大鼠表现出牙槽骨吸收加剧、炎症过度活跃和牙周 AMPK 活性降低。AMPK 激动剂的注射减轻了 2 型糖尿病引起的牙周炎症和牙槽骨吸收,从而使正畸牙移动距离正常化。我们的研究表明,2 型糖尿病降低了牙周 AMPK 活性,导致过度炎症增加破骨细胞形成和牙槽骨吸收,这可以通过 AMPK 激活来逆转。

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The onset of adenosine monophosphate-activated protein kinase activity on orthodontic tooth movement in rats with type 2 diabetes.2 型糖尿病大鼠正畸牙齿移动时腺苷一磷酸激活蛋白激酶活性的起始。
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