期刊
FRONTIERS IN PHYSIOLOGY
卷 9, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fphys.2018.00024
关键词
TRIM31; glucose metabolism; insulin resistance; gut microbiota; inflammation
类别
资金
- National 973 Basic Research Program of China [2013CB530703, 2015CB553604]
- Key Research and Development Plan of Shandong Province [2015GSF118133]
- National key R D plan [2016YFC1300403]
- National Natural Science Foundation of China [31770977, 81425004, 81770442, 61331001, 81530014, 81320108004, 81400284, 91339109, 81270350, 31400771]
- Program of Introducing Talents of Discipline to Universities [B07035]
- State Key Program of National Natural Science of China [61331001, 81530014]
- International Collaboration and Exchange Program of China [81320108004]
- Natural Science Foundation of Shandong Province [ZR2014CQ004]
- Clinical Medicine Science and Technology Innovation Plan of Jinan Science and Technology Bureau [201602157, 201506002]
- Shenzhen Science and Technology Research and Development Fund [JCYJ20160331183804137]
- Science and Technology Project of Guangdong Province [2017A020215005]
Tripartite motif-containing protein 31 (TRIM31), an E3 ubiquitin ligase of the tripartite motif family, plays an important role in the innate immune response. It can reduce the activity of the nucleotide-binding oligomerization domain-like receptor (NLR) family pyrin domain containing 3 (NLRP3) inflammasome. However, little information is about glucose metabolic health of TRIM31-deficient mice, and investigations about gut microbiota in TRIM31-deficient mice is limited. Thus, we aimed to compare glucose metabolic parameters, gut microbiota composition and inflammatory cytokine levels between TRIM31(-/-) and wild-type (WT) mice, and further investigate whether or not certain gut microbiota taxon correlates with specific metabolic parameters and inflammation cytokines in TRIM31-deficient mice. TRIM31(-/-) mice showed glucose intolerance and insulin resistance, with a significant difference in gut microbiota composition, characterized by increased abundance of Prevotellaceae and Veillonellaceae. TRIM31(-/-) mice with impaired glucose metabolism was accompanied by elevated serum tumor necrosis factor-alpha (TNF-alpha) and interleukin 1 beta W (IL-1 beta) concentrations, as well as upregulated caecal TNF-alpha, IL-1 beta, caspase-1, and NLRP3 expressions. Furthermore, elevated p-IRS-1/IRS-1 protein expression, and decreased Akt Thr308 phosphorylation were observed in TRIM31(-/-) mice. Prevotellaceae abundance was positively associated with caecal IL-1 beta mRNA expression, and Veillonellaceae was associated with higher TNF-a mRNA expression and serum insulin concentration. In conclusion, our study is novel in showing that TRIM31 deficiency is associated with impaired glucose metabolism and disrupted gut microbiota in mice. This study contributes to the theoretical foundation on the potential relationship between TRIM31 deficiency and the development of abnormal glucose metabolism.
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