牙龈卟啉单胞菌
牙周炎
脂肪组织
白色脂肪组织
脂联素
生物
核梭杆菌
胰岛素抵抗
牙周病原体
内分泌学
免疫学
内科学
胰岛素
医学
作者
Yiying Liu,Bin Cui,Ping Zhang,Song Xiao,Dingyu Duan,Yi Ding
标识
DOI:10.1177/00220345231211210
摘要
Recent studies have indicated that periodontitis promotes metabolic dysregulation and insulin resistance by affecting the function of white adipose tissue (WAT). However, the mechanisms linking periodontitis to adipose tissue dysfunction still need to be explored. Extracellular vesicles (EVs) deliver messages to distal sites and regulate their function. Also, recent studies have shown that periodontitis changes the composition of EVs in body fluids and that EVs might be one of the mechanisms underlying the relationship between periodontitis and insulin resistance. Herein, we explored the impact of polymicrobial oral infection with periodontal pathogens on the function of WAT and the role of gingival EVs (gEVs) in the process. Mice were subjected to oral inoculation with 10 9 Porphyromonas gingivalis and 10 8 Fusobacterium nucleatum every other day for 14 wk. This prolonged bacterial infection induced WAT dysfunction, characterized by reduced levels of AKT phosphorylation, adiponectin, leptin, and genes associated with adipogenesis and lipogenesis. We successfully isolated gEVs with satisfactory yield and purity. The RNA sequencing results showed that the differentially expressed microRNAs in the gEVs of mice with polymicrobial oral infection were involved in insulin signaling and adipose tissue function. Notably, our in vitro experiments and RNA sequencing results revealed the functional similarities between gEVs and plasma-derived EVs. Furthermore, intraperitoneal injection with gEVs derived from mice with oral infection induced the dysfunction of WAT in healthy mice. Overall, our findings provide evidence for the influence of polymicrobial oral infection on WAT function and propose gEVs as a novel pathway through which periodontal infection may exert its effects on WAT.
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