高脂饮食刺激丁酸代谢紊乱,改变微生物群,加重胶原蛋白诱发关节炎大鼠的炎症反应。

IF 3.9 2区 医学 Q2 NUTRITION & DIETETICS Nutrition & Metabolism Pub Date : 2024-11-19 DOI:10.1186/s12986-024-00869-x
Yantong Liu, Yang Zhang, Jie Zhang, Shuang Ren, Qi Cao, Hongxi Kong, Qiangqiang Xu, Ruoshi Liu
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引用次数: 0

摘要

背景:研究表明,肥胖可能与类风湿性关节炎(RA)有关。此外,肠道微生物群及其代谢产物的菌群失调也与 RA 和肥胖的发生和发展有关。本研究探讨了高脂饮食(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了其机制:根据饮食和模型,大鼠被分为正常组(Con)、CIA模型组、HFD组(HFD)和HFD + CIA组(HCIA)。根据关节炎指数(AI)、体重、血脂水平和炎症细胞因子,研究 HFD 对 CIA 大鼠关节炎的影响。采用 16S rRNA 扩增子测序和液相色谱-质谱法(LC-MS)探讨肠道微生物群和短链脂肪酸(SCFAs)的变化:结果:HCIA组的AI评分、炎症细胞因子和骨破坏参数明显高于其他三组。16S rRNA 扩增子测序和代谢组学研究结果显示,与其他三组相比,HCIA 组中 g_Muribaculaceae 和丁酸的表达量减少。斯皮尔曼和线性相关分析表明,g_Muribaculaceae丰度与丁酸水平呈正相关:结论:HFD 刺激了 CIA 大鼠的丁酸代谢紊乱、微生物群改变并加剧了炎症反应。
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High-fat diet stimulated butyric acid metabolism dysbiosis, altered microbiota, and aggravated inflammatory response in collagen-induced arthritis rats.

Background: 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.

Methods: 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).

Results: 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.

Conclusions: HFD stimulated butyric acid metabolism dysbiosis, altered microbiota, and aggravated inflammatory response in CIA rats.

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来源期刊
Nutrition & Metabolism
Nutrition & Metabolism 医学-营养学
CiteScore
8.40
自引率
0.00%
发文量
78
审稿时长
4-8 weeks
期刊介绍: Nutrition & Metabolism publishes studies with a clear focus on nutrition and metabolism with applications ranging from nutrition needs, exercise physiology, clinical and population studies, as well as the underlying mechanisms in these aspects. The areas of interest for Nutrition & Metabolism encompass studies in molecular nutrition in the context of obesity, diabetes, lipedemias, metabolic syndrome and exercise physiology. Manuscripts related to molecular, cellular and human metabolism, nutrient sensing and nutrient–gene interactions are also in interest, as are submissions that have employed new and innovative strategies like metabolomics/lipidomics or other omic-based biomarkers to predict nutritional status and metabolic diseases. Key areas we wish to encourage submissions from include: -how diet and specific nutrients interact with genes, proteins or metabolites to influence metabolic phenotypes and disease outcomes; -the role of epigenetic factors and the microbiome in the pathogenesis of metabolic diseases and their influence on metabolic responses to diet and food components; -how diet and other environmental factors affect epigenetics and microbiota; the extent to which genetic and nongenetic factors modify personal metabolic responses to diet and food compositions and the mechanisms involved; -how specific biologic networks and nutrient sensing mechanisms attribute to metabolic variability.
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