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Lactobacillus rhamnosus GG ameliorates hyperuricemia in a novel model. 2024
Yang Fu, and
Yong-Song Chen, and
Dai-Yang Xia, and
Xiao-Dan Luo, and
Hao-Tong Luo, and
Jie Pan, and
Wei-Qing Ma, and
Jin-Ze Li, and
Qian-Yuan Mo, and
Qiang Tu, and
Meng-Meng Li, and
Yue Zhao, and
Yu Li, and
Yi-Teng Huang, and
Zhi-Xian Chen, and
Zhen-Jun Li, and
Lukuyu Bernard, and
Michel Dione, and
You-Ming Zhang, and
Kai Miao, and
Jian-Ying Chen, and
Shan-Shan Zhu, and
Jie Ren, and
Ling-Juan Zhou, and
Xian-Zhi Jiang, and
Juan Chen, and
Zhen-Ping Lin, and
Jun-Peng Chen, and
Hui Ye, and
Qing-Yun Cao, and
Yong-Wen Zhu, and
Lin Yang, and
Xue Wang, and
Wen-Ce Wang
State Key Laboratory of Swine and Poultry Breeding Industry, College of Animal Science, South China Agricultural University, Guangzhou, 510642, China.
Hyperuricemia (HUA) is a metabolic syndrome caused by abnormal purine metabolism. Although recent studies have noted a relationship between the gut microbiota and gout, whether the microbiota could ameliorate HUA-associated systemic purine metabolism remains unclear. In this study, we constructed a novel model of HUA in geese and investigated the mechanism by which Lactobacillus rhamnosus GG (LGG) could have beneficial effects on HUA. The administration of antibiotics and fecal microbiota transplantation (FMT) experiments were used in this HUA goose model. The effects of LGG and its metabolites on HUA were evaluated in vivo and in vitro. Heterogeneous expression and gene knockout of LGG revealed the mechanism of LGG. Multi-omics analysis revealed that the Lactobacillus genus is associated with changes in purine metabolism in HUA. This study showed that LGG and its metabolites could alleviate HUA through the gut-liver-kidney axis. Whole-genome analysis, heterogeneous expression, and gene knockout of LGG enzymes ABC-type multidrug transport system (ABCT), inosine-uridine nucleoside N-ribohydrolase (iunH), and xanthine permease (pbuX) demonstrated the function of nucleoside degradation in LGG. Multi-omics and a correlation analysis in HUA patients and this goose model revealed that a serum proline deficiency, as well as changes in Collinsella and Lactobacillus, may be associated with the occurrence of HUA. Our findings demonstrated the potential of a goose model of diet-induced HUA, and LGG and proline could be promising therapies for HUA.
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Journal of microbiology, immunology, and infection = Wei mian yu gan ran za zhi,
