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对高脂饮食诱导肥胖小鼠中抗生素抗性基因增殖探索的见解。

An insight into the exploration of proliferation of antibiotic resistance genes in high-fat diet induced obesity mice.

作者信息

Wang Rui, Chen Dawei, Wang Fang, Fan Xiuqin, Fan Chaonan, Tang Tiantian, Li Ping, Yang Mengyi, Zhao Yunfeng, Qi Kemin

机构信息

Laboratory of Nutrition and Development,Beijing Pediatric Research Institute,Key Laboratory of Major Diseases in Children,Ministry of Education,Beijing Children's Hospital,Capital Medical University,National Center for Children's Health, Beijing 100045, PR China.

NHC Key Laboratory of Food Safety Risk Assessment, Chinese Academy of Medical Science Research Unit (No. 2019RU014), China National Center for Food Safety Risk Assessment, PR China.

出版信息

Genomics. 2021 Jul;113(4):2503-2512. doi: 10.1016/j.ygeno.2021.05.041. Epub 2021 Jun 2.

DOI:10.1016/j.ygeno.2021.05.041
PMID:34089783
Abstract

Using mice as an animal model, we first demonstrated the significant proliferation of ARGs and the change of mobile genetic elements (MGEs) in high-fat diet induced obesity (DIO) mice, which the ermB and tnpA-03 genes mostly increased, illuminating that DIO could enrich the abundance of ARGs. Additionally, Lactobacillus sharply increased in the DIO mice and might contribute to the proliferation of ARGs and dramatical change of MGEs in the HFD groups. Finally, procrustes analysis showed the explanatory variables of the MGEs, the metabolites, and the microbial communities for the ARGs accounted for 94.3%, 53.4%, and 68.1%, respectively, and implying that MGEs might be the most direct factor affecting ARGs, and microbiota could be the main driver of the proliferation of ARGs in the DIO mice.

摘要

以小鼠作为动物模型,我们首先证明了在高脂饮食诱导的肥胖(DIO)小鼠中,抗生素抗性基因(ARGs)显著增殖以及移动遗传元件(MGEs)发生变化,其中ermB和tnpA - 03基因大多增加,这表明DIO可使ARGs丰度增加。此外,DIO小鼠中乳酸杆菌急剧增加,可能导致高脂饮食组中ARGs增殖和MGEs发生显著变化。最后,普罗克汝斯忒斯分析表明,MGEs、代谢物和微生物群落对ARGs的解释变量分别占94.3%、53.4%和68.1%,这意味着MGEs可能是影响ARGs的最直接因素,而微生物群可能是DIO小鼠中ARGs增殖的主要驱动因素。

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