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Inulin Can Alleviate Metabolism Disorders in ob/ob Mice by Partially Restoring Leptin-related Pathways Mediated by Gut Microbiota

摘要Inulin has been used as a prebiotic to alleviate glucose and lipid metabolism disorders in mice and humans by modulating the gut microbiota. However, the mechanism underlying the alle-viation of metabolic disorders by inulin through interactions between the gut microbiota and host cells is unclear. We use ob/ob mice as a model to study the effect of inulin on the cecal microbiota by 16S rRNA gene amplicon sequencing and its interaction with host cells by transcriptomics. The inulin-supplemented diet improved glucose and lipid metabolism disorder parameters in ob/ob mice, alleviating fat accumulation and glucose intolerance. Theαdiversity of gut microbial community of ob/ob mice was reduced after inulin treatment, while theβdiversity tended to return to the level of wild type mice. Interestingly, Prevotellaceae UCG 001 (family Prevotellaceae) was obviously enriched after inulin treatment. A comparative analysis of the gene expression profile showed that the cecal transcriptome was changed in leptin gene deficiency mice, whereas the inulin-supplemented diet partially reversed the changes in leptin gene-related signaling pathways, especially AMPK sig-naling pathway, where the levels of gene expression became comparable to those in wild type mice. Further analysis indicated that Prevotellaceae UCG 001 was positively correlated with the AMPK signaling pathway, which was negatively correlated with markers of glycolipid metabolism disor-ders. Our results suggest that the inulin-supplemented diet alleviates glucose and lipid metabolism disorders by partially restoring leptin related pathways mediated by gut microbiota.

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作者单位 CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China;Savaid Medical School, University of Chinese Academy of Sciences, Beijing 100049, China;Beijing Key Laboratory of Microbial Drug Resistance and Resistome, Beijing 100101, China [1] CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China [2] CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China;Beijing Key Laboratory of Microbial Drug Resistance and Resistome, Beijing 100101, China [3] College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China [4] CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China;Savaid Medical School, University of Chinese Academy of Sciences, Beijing 100049, China [5] State Key Laboratory of Animal Nutrition, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China [6] CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China;Savaid Medical School, University of Chinese Academy of Sciences, Beijing 100049, China;Beijing Key Laboratory of Microbial Drug Resistance and Resistome, Beijing 100101, China;Department of Pathogenic Biology, School of Basic Medical Sciences, Southwest Medical University, Luzhou 646000, China [7]
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发布时间 2019-06-21(万方平台首次上网日期,不代表论文的发表时间)
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