Department of Implantology, Shanghai Stomatological Hospital and School of Stomatology, Fudan University, Shanghai, China.
Shanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Fudan University, Shanghai, China.
Front Cell Infect Microbiol. 2022 Apr 7;12:858902. doi: 10.3389/fcimb.2022.858902. eCollection 2022.
Periodontitis has been demonstrated to increase the risk of metabolic syndrome (MetS), but the underlying mechanism remains unclear. Recent studies have indicated periodontopathic bacteria such as could induce gut microbiota (GM) dysbiosis and aggravate metabolic disorders. However, the effects of microbial metabolites have barely been evaluated. Here, we investigated the alteration of serum metabolome with -induced metabolic disorders, and explored the correlations of GM and serum metabolites. In this study, we orally administered ATCC33277 to C57BL/6 mice and performed metagenomic sequencing and untargeted metabolomics with fecal samples and serum collection. experiments showed a higher proportion of fat mass and worse glucose tolerance in -administered mice, accompanied with an increase of adipose inflammation and gut permeability, which was similar to HFD-induced obese mice. Metagenomic sequencing indicated a compositional and functional alteration of GM. Untargeted metabolomics revealed an alteration of metabolites in -administered mice, and most of them were engaged in metabolic pathways, such as tryptophan metabolism and choline metabolism. Correlation analysis between GM and serum metabolome indicated strong relativity with administration. These results demonstrated some specific microbiota-derived metabolites in the pathogenesis of -induced metabolic disorders, providing promising targets for the development of novel treatment strategies for MetS.
牙周炎已被证明会增加代谢综合征（MetS）的风险，但潜在机制仍不清楚。最近的研究表明，牙周病细菌如 可能会诱导肠道微生物群（GM）失调并加重代谢紊乱。然而，微生物代谢产物的影响几乎没有被评估。在这里，我们研究了 - 诱导的代谢紊乱对血清代谢组的改变，并探讨了 GM 和血清代谢物的相关性。在这项研究中，我们给 C57BL/6 小鼠口服 ATCC33277，并对粪便样本和血清采集进行宏基因组测序和非靶向代谢组学分析。 实验表明，给予 的小鼠的脂肪量比例更高，葡萄糖耐量更差，伴随着脂肪炎症和肠道通透性增加，这与 HFD 诱导的肥胖小鼠相似。宏基因组测序表明 GM 的组成和功能发生了改变。非靶向代谢组学揭示了给予 的小鼠代谢物的改变，其中大多数参与了代谢途径，如色氨酸代谢和胆碱代谢。GM 和血清代谢组之间的相关性分析表明与 给药有很强的相关性。这些结果表明，在 - 诱导的代谢紊乱发病机制中存在一些特定的微生物衍生代谢物，为代谢综合征的新型治疗策略的开发提供了有希望的靶点。
