Liu Yantong, Zhang Yang, Zhang Jie, Ren Shuang, Cao Qi, Kong Hongxi, Xu Qiangqiang, Liu Ruoshi
Department of Traditional Chinese Medicine, The First Hospital of China Medical University, Shenyang, 110001, China.
School of Acupuncture-Moxibustion and Tuina, Liaoning University of Traditional Chinese Medicine, Shenyang, 110001, China.
Nutr Metab (Lond). 2024 Nov 19;21(1):95. doi: 10.1186/s12986-024-00869-x.
Research has demonstrated that obesity may be associated with rheumatoid arthritis (RA). In addition, Dysbiosis of intestinal microbiota and their metabolites has been linked to the occurrence and development of RA and obesity. However, the mechanism by which obesity affects RA remains unclear.In this study, we explored the impact of high fat diet(HFD) on collagen-induced arthritis (CIA) rats and revealed its mechanisms based on gut microbiota and metabolomics.
Based on diet and modeling, rats were divided into normal group (Con), CIA model group, HFD group (HFD), and HFD + CIA group (HCIA). The effect of HFD on arthritis in CIA rats were investigated based on the arthritis index (AI), weight, blood lipid levels, and inflammatory cytokines. Moreover, HE staining and micro-CT were performed to evaluated the effect of HFD on the pathology of joints and synovial tissues in CIA rats.16S rRNA amplicon sequencing and liquid chromatography-mass spectrometry (LC-MS) were employed to explore changes in gut microbiota and short-chain fatty acids (SCFAs).
The AI scores, inflammatory cytokines and bone destruction parameters in the HCIA group were significantly higher than those in the other three groups. The results of 16S rRNA amplicon sequencing and metabolomics showed that compared with the other three groups, the expression of g_Muribaculaceae and butyric acid were reduced in the HCIA group. Spearman and linear correlation analyses revealed a positive correlation between g_Muribaculaceae abundance and butyric acid levels.
HFD stimulated butyric acid metabolism dysbiosis, altered microbiota, and aggravated inflammatory response in CIA rats.
研究表明肥胖可能与类风湿关节炎(RA)相关。此外,肠道微生物群及其代谢产物的失调与RA和肥胖的发生发展有关。然而,肥胖影响RA的机制尚不清楚。在本研究中,我们探讨了高脂饮食(HFD)对胶原诱导性关节炎(CIA)大鼠的影响,并基于肠道微生物群和代谢组学揭示其机制。
根据饮食和造模情况,将大鼠分为正常组(Con)、CIA模型组、高脂饮食组(HFD)和高脂饮食+CIA组(HCIA)。基于关节炎指数(AI)、体重、血脂水平和炎性细胞因子,研究HFD对CIA大鼠关节炎的影响。此外,进行苏木精-伊红(HE)染色和显微CT以评估HFD对CIA大鼠关节和滑膜组织病理学的影响。采用16S rRNA扩增子测序和液相色谱-质谱联用(LC-MS)技术探讨肠道微生物群和短链脂肪酸(SCFAs)的变化。
HCIA组的AI评分、炎性细胞因子和骨破坏参数显著高于其他三组。16S rRNA扩增子测序和代谢组学结果显示,与其他三组相比,HCIA组中g_ Muribaculaceae的表达和丁酸含量降低。Spearman和线性相关性分析显示g_ Muribaculaceae丰度与丁酸水平呈正相关。
高脂饮食刺激丁酸代谢失调,改变微生物群,并加重CIA大鼠的炎症反应。