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首页> 外文期刊>The Journal of Nutritional Biochemistry >Gut microbiota-me diate d xanthine metabolism is associate d with resistance to high-fat diet-induced obesity
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Gut microbiota-me diate d xanthine metabolism is associate d with resistance to high-fat diet-induced obesity

机译：肠道微生物瘤介导的黄嘌呤代谢与耐高脂饮食诱导的肥胖有关

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Resistance to high-fat diet-induced obesity (DIR) has been observed in mice fed a high-fat diet and may provide a potential approach for anti-obesity drug discovery. However, the metabolic status, gut microbiota composition, and its associations with DIR are still unclear. Here, ultraperformance liquid chromatography-tandem mass spectrometry-based urinary metabolomic and 16S rRNA gene sequencing-based fecal microbiome analyses were conducted to investigate the relationship between metabolic profile, gut microbiota composition, and body weight of C57BL/6J mice on chow or a high-fat diet for 8 weeks. PICRUSt analysis of 16S rRNA gene sequences predicted the functional metagenomes of gut bacteria. The results demonstrated that feeding a high-fat diet increased body weight and fasting blood glucose of high-fat diet-induced obesity (DIO) mice and altered the host-microbial co-metabolism and gut microbiota composition. In DIR mice, high-fat diet did not increase body weight while fasting blood glucose was increased significantly compared to chow fed mice. In DIR mice, the urinary metabolic pattern was shifted to a distinct direction compared to DIO mice, which was mainly contributed by xanthine. Moreover, high-fat diet caused gut microbiota dysbiosis in both DIO and DIR mice, but in DIR mice, the abundance of Bifidobacteriaceae, Roseburia, and Escherichia was not affected compared to mice fed a chow diet, which played an important role in the pathway coverage of FormylTHF biosynthesis I. Meanwhile, xanthine and pathway coverage of FormylTHF biosynthesis I showed significant positive correlations with mouse body weight. These findings suggest that gut microbiota-mediated xanthine metabolism correlates with resistance to high-fat DIO. (C) 2020 Elsevier Inc. All rights reserved.
机译：在喂食高脂饮食的小鼠中观察到对高脂饮食诱导的肥胖（DIR）的抵抗，这可能为发现抗肥胖药物提供了一种潜在的方法。然而，代谢状态、肠道微生物群组成及其与DIR的关系仍不清楚。在这里，进行了基于超高效液相色谱-串联质谱的尿代谢组学和基于16S rRNA基因测序的粪便微生物组学分析，以研究喂食食物或高脂饮食8周的C57BL/6J小鼠的代谢特征、肠道微生物组分和体重之间的关系。对16S rRNA基因序列的微电泳分析预测了肠道细菌的功能性亚基因组。结果表明，喂食高脂饮食可增加高脂饮食诱导肥胖（DIO）小鼠的体重和空腹血糖，并改变宿主微生物共代谢和肠道微生物群组成。在DIR小鼠中，与周饲小鼠相比，高脂饮食没有增加体重，而空腹血糖显著升高。在DIR小鼠中，与主要由黄嘌呤贡献的DIO小鼠相比，尿液代谢模式发生了明显的改变。此外，高脂饮食导致DIO和DIR小鼠肠道微生物群失调，但在DIR小鼠中，与喂食周粮的小鼠相比，双歧杆菌科、Roseburia和大肠杆菌的丰度没有受到影响，这在甲酰THF生物合成I的途径覆盖中发挥了重要作用，甲酰THF生物合成I的黄嘌呤和途径覆盖率与小鼠体重呈显著正相关。这些发现表明，肠道微生物群介导的黄嘌呤代谢与对高脂DIO的耐药性相关。（C） 2020爱思唯尔公司版权所有。

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