Université de La Réunion, Inserm, UMR 1188 Diabète Athérothrombose Thérapies Réunion Océan Indien (DéTROI), 97490 Saint-Denis de La Réunion, France.
Nutrition and Obesity, Systemic Approaches (NutriOmics), INSERM, Sorbonne Université, 75013 Paris, France.
Biomolecules. 2022 Feb 28;12(3):378. doi: 10.3390/biom12030378.
Type 2 diabetes is a metabolic disease mainly associated with insulin resistance during obesity and constitutes a major public health problem worldwide. A strong link has been established between type 2 diabetes and periodontitis, an infectious dental disease characterized by chronic inflammation and destruction of the tooth-supporting tissue or periodontium. However, the molecular mechanisms linking periodontal bacteria and insulin resistance remain poorly elucidated. This study aims to summarize the mechanisms possibly involved based on in vivo and in vitro studies and targets them for innovative therapies. Indeed, during periodontitis, inflammatory lesions of the periodontal tissue may allow periodontal bacteria to disseminate into the bloodstream and reach tissues, including adipose tissue and skeletal muscles that store glucose in response to insulin. Locally, periodontal bacteria and their components, such as lipopolysaccharides and gingipains, may deregulate inflammatory pathways, altering the production of pro-inflammatory cytokines/chemokines. Moreover, periodontal bacteria may promote ROS overproduction via downregulation of the enzymatic antioxidant defense system, leading to oxidative stress. Crosstalk between players of inflammation and oxidative stress contributes to disruption of the insulin signaling pathway and promotes insulin resistance. In parallel, periodontal bacteria alter glucose and lipid metabolism in the liver and deregulate insulin production by pancreatic β-cells, contributing to hyperglycemia. Interestingly, therapeutic management of periodontitis reduces systemic inflammation markers and ameliorates insulin sensitivity in type 2 diabetic patients. Of note, plant polyphenols exert anti-inflammatory and antioxidant activities as well as insulin-sensitizing and anti-bacterial actions. Thus, polyphenol-based therapies are of high interest for helping to counteract the deleterious effects of periodontal bacteria and improve insulin resistance.
2 型糖尿病是一种代谢疾病,主要与肥胖期间的胰岛素抵抗有关,是全球范围内的一个主要公共卫生问题。2 型糖尿病与牙周炎之间存在很强的关联,牙周炎是一种以慢性炎症和牙齿支持组织(即牙周组织)破坏为特征的感染性牙科疾病。然而,牙周细菌与胰岛素抵抗之间的分子机制仍未得到充分阐明。本研究旨在根据体内和体外研究总结可能涉及的机制,并将其作为创新疗法的靶点。事实上,在牙周炎期间,牙周组织的炎症病变可能使牙周细菌扩散到血液中并到达组织中,包括储存葡萄糖以响应胰岛素的脂肪组织和骨骼肌。在局部,牙周细菌及其成分(如脂多糖和牙龈蛋白酶)可能会使炎症途径失调,改变促炎细胞因子/趋化因子的产生。此外,牙周细菌可能通过下调酶抗氧化防御系统导致活性氧(ROS)过度产生,从而导致氧化应激。炎症和氧化应激参与者之间的串扰会破坏胰岛素信号通路并促进胰岛素抵抗。同时,牙周细菌会改变肝脏中的葡萄糖和脂质代谢,并使胰腺β细胞中的胰岛素产生失调,导致高血糖。有趣的是,牙周炎的治疗管理可降低 2 型糖尿病患者的全身炎症标志物并改善胰岛素敏感性。值得注意的是,植物多酚具有抗炎、抗氧化作用以及胰岛素增敏和抗菌作用。因此,基于多酚的治疗方法具有很高的应用价值,可以帮助抵消牙周细菌的有害影响并改善胰岛素抵抗。