Lactobacillus reuteri ZJ617 attenuates metabolic syndrome via microbiota-derived spermidine

被引:0
|
作者
Ma, Yanfei [1 ]
Zhong, Yifan [1 ]
Tang, Wenjie [1 ]
Valencak, Teresa G. [1 ]
Liu, Jingliang [1 ]
Deng, Zhaoxi [1 ]
Mao, Jiangdi [1 ]
Liu, Daren [2 ]
Wang, Shanshan [1 ]
Wang, Yuhao [3 ]
Wang, Haifeng [1 ]
机构
[1] Zhejiang Univ, Coll Anim Sci, Key Lab Mol Anim Nutr, Minist Educ, Hangzhou 310058, Zhejiang, Peoples R China
[2] Zhejiang Univ, Affiliated Hosp 2, Hangzhou 310009, Zhejiang, Peoples R China
[3] Zhejiang Univ, Inst Translat Med, Sch Med, Hangzhou 310029, Zhejiang, Peoples R China
基金
国家重点研发计划;
关键词
BROWN ADIPOSE-TISSUE; POLYAMINE; DECARBOXYLASE; INHIBITION; BERENIL; OBESITY; FAT; RNA;
D O I
10.1038/s41467-025-56105-4
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Metabolic syndrome (MetS) is a difficult-to-manage disease that poses a significant risk to human health. Here, we show that the supplementation of Lactobacillus reuteri ZJ617 ameliorates symptoms of MetS in mice induced by the high-fat diet. L. reuteri ZJ617 modulates host metabolism by interacting with the microbiome, resulting in the production of spermidine synthesized by the microbiota. L. reuteri ZJ617 serves as a source of substrates for the microbiota to synthesize spermidine, hence preventing the decline of bacteria responsible for spermidine production. Spermidine treatment mimics the metabolic effects of L. reuteri ZJ617, whereas pharmacological inhibition of spermidine biosynthesis in mice abolishes these benefits. Our findings reveal the mechanism by which L. reuteri ZJ617 alleviates MetS symptoms and provide support for its potential use as a probiotic for promoting metabolic health.
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页数:15
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