alleviates the obesity of ob/ob mice and improves their intestinal microbiota and bile acid metabolism.

Food Funct

Key Laboratory of Animal Molecular Nutrition of Education of Ministry, National Engineering Laboratory of Biological Feed Safety and Pollution Prevention and Control, Key Laboratory of Animal Feed and Nutrition of Zhejiang Province, Institute of Animal Nutrition and Feed Sciences, College of Animal Sciences, Zhejiang University, Hangzhou, Zhejiang 310058, China.

Published: May 2022

Dietary interventions with probiotics have been widely reported to be effective in regulating obesity, and the intestinal microbiota is considered to be an important environmental factor. However, few reports focus on the interactions of microbiota-metabolites-phenotypic variables in ob/ob mice, and they have not been characterized in great detail. In this study, we investigated the effects of SC06 on obesity, the intestinal microbiota and the bile acid metabolism of ob/ob mice using biochemical testing, histochemical staining, high-throughput sequencing of the 16S rRNA gene, LC-MS/MS analysis and qRT-PCR. The results showed that SC06 ameliorated the fat mass percentage, hepatic steatosis and liver lipid metabolism disorders and reshaped the gut microbiota and metabolites in male ob/ob mice, specifically deceasing , , , , , , , , , , and and increasing , and . Meanwhile, SC06 treatment groups had lower ibuprofen and higher glycodeoxycholic acid and 7-dehydrocholesterol. Correlation analysis further clarified the relationships between compositional changes in the microbiota and alterations in the metabolites and phenotypes of ob/ob mice. Moreover, SC06 downregulated bile acid synthesis, export and re-absorption in the liver and increased ileum re-absorption into the blood in ob/ob mice, which may be mediated by the FXR-SHP/FGF15 signaling pathway. These results suggest that SC06 can ameliorate obesity in male ob/ob mice by reshaping the intestinal microbial composition, changing metabolites and regulating bile acid metabolism the FXR signaling pathway.

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Source
http://dx.doi.org/10.1039/d1fo03170hDOI Listing

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