Isolated exopolysaccharides from Lactobacillus rhamnosus GG alleviated adipogenesis mediated by TLR2 in mice

被引:73
作者
Zhang, Zhen [1 ]
Zhou, Zhigang [1 ]
Li, Yu [1 ]
Zhou, Linkang [2 ,3 ]
Ding, Qianwen [1 ]
Xu, Li [1 ,2 ,3 ]
机构
[1] Chinese Acad Agr Sci, Feed Res Inst, Key Lab Feed Biotechnol, Minist Agr, Beijing, Peoples R China
[2] Tsinghua Univ, Sch Life Sci, MOE Key Lab Bioinformat, Beijing 100084, Peoples R China
[3] Tsinghua Univ, Sch Life Sci, Tsinghua Peking Ctr Life Sci, Beijing 100084, Peoples R China
基金
中国国家自然科学基金;
关键词
GUT MICROBIOTA; STRUCTURAL-CHARACTERIZATION; BIFIDOBACTERIUM-ANIMALIS; OBESITY; ALPHA; POLYSACCHARIDES; WEIGHT; RECEPTOR; ACID; INFLAMMATION;
D O I
10.1038/srep36083
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
The fibroblast cell line of 3T3-L1 was used as a cell model for screening and evaluating the feasibility of probiotic components in improving animal lipid metabolisms. The extracts from 12 Lactobacillus strains caused significantly reduced triacylglycerol (TAG) accumulation but with severe inflammation induction in 3T3-L1 adipocytes. Interestingly, exopolysaccharides (EPS) from LGG (Lactobacillus rhamnosus GG) significantly decreased the TAG accumulation without any inflammation. The anti-obesity effect of EPS was confirmed in high-fat-diets feeding mice. Fat pads of mice injected with EPS (50 mg/kg) every two days for two weeks were significantly reduced with much smaller adipocytes, compared with the counterparts. The levels of TAG and cholesterol ester in liver, as well as serum TAG, were decreased in EPS injected mice. In addition, down-regulated inflammation was observed in adipose tissue and liver. Interestingly, the expression of TLR2 in adipose tissue and 3T3-L1 cells was significantly increased by EPS addition. Moreover, the reverse of TAG accumulation in TLR2 knockdown 3T3-L1 in the presence of EPS confirmed that the inhibition effect of EPS on adipogenesis was mediated by TLR2. EPS from LGG has the potential for therapeutic development to intervene lipid metabolic disorders in mammals.
引用
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页数:14
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