非酒精性脂肪肝
牙周炎
肠道菌群
失调
微生物群
内科学
内分泌学
脂肪肝
背景(考古学)
医学
生物
免疫学
疾病
生物信息学
古生物学
作者
Min Wang,Lili Li,Jun Qian,Nannan Wang,Junmin Bao,Jing Lü,Fa‐Ming Chen,Yanfen Li,Yangheng Zhang,Fuhua Yan
出处
期刊:iScience
[Elsevier]
日期:2023-04-01
卷期号:26 (4): 106346-106346
被引量:5
标识
DOI:10.1016/j.isci.2023.106346
摘要
Periodontitis may aggravate the development of nonalcoholic fatty liver disease (NAFLD); however, the precise mechanism is unknown. In this study, salivary microbiota collected from patients with periodontitis was transferred intragastrically to obese mice induced by high-fat diet. Microbiomics and metabolomics analysis were performed to assess the influence of periodontitis salivary microbiota on gut microbiome and liver metabolism. Periodontitis salivary microbiota altered gut microbiota composition and exacerbated intestinal barrier dysfunction in obese mice. Subsequently, the bacterial lipopolysaccharide transported to liver may activate the toll-like receptor 4 signaling and cause the release of pro-inflammatory factors. Moreover, the tryptophan-kynurenine-AhR signal axis was upregulated in liver, which may be related to aggravated hepatic steatosis and glucolipid metabolism dysregulation during NAFLD development. This study indicated that in the context of obesity, periodontitis salivary microbiota may aggravate the pathological progression of NAFLD, in which the tryptophan-AhR pathway may play a key role.
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