Improvement on metabolic syndrome in high fat diet-induced obese mice through modulation of gut microbiota by sangguayin decoction

Published on Jan 1, 2020in Journal of Ethnopharmacology3.414
· DOI :10.1016/j.jep.2019.112225
Junping Zheng1
Estimated H-index: 1
(Hubei University of Chinese Medicine),
Jing Zhang1
Estimated H-index: 1
(Hubei University of Chinese Medicine)
+ 6 AuthorsHongtao Liu1
Estimated H-index: 1
(Hubei University of Chinese Medicine)
Abstract Ethnopharmacological relevance Our previous research found that Sangguayin (SGY) deccoction made by four dietary and medicinal plant components (Leaf of Morus alba L., Root of Pueraria lobata (Willd.) Ohwi., Root of Dioscorea opposita Thunb. and Fruit of Momordica charantia L.) showed significant anti-diabetic effects on db/db mice and high fat diet induced obese mice. Nevertheless, it remained unclear what the role of gut microbiota in the hypoglycaemia effects of SGY. Aims of the study This study aimed to examine the beneficial effects of Sangguayin Deccoction against metabolic syndrome and and its regulating role in gut microbiota and hepatic metabolome. Materials and methods C57BL/6J mice were divided to a normal chow diet (NCD), high-fat diet (HFD), and high-fat diet with Sangguayin Decoction (HFD-SGY, oral dose of 250 mg/kg/d) for 16 weeks. Next generation sequencing was applied for analyzing the gut microbial community of colonic contents. Further, untargeted metabolomic analysis based on LC-MS was used for determining the changes of hepatic metabolites. Hepatic genes expression were measured by quantitative PCR. Results SGY supplement decreased blood glucose level and glucose intolerance. Illumina MiSeq sequencing revealed that SGY increased Verrucomicrobia phylum, resulting in a bloom of Akkermansia, and eventually upregulated the contents of Lachoclostridium and Roseburia. Additionally, dietary SGY decreased bacteria including Faecalibaculum, and Blautia. Moreover, the hepatic lipid metabolism was notably altered by SGY treatment. The oxidation of glutamione metabolism idecreasees, production of poly-unsaturated fatty acid (PUFA) got significant increase in liver tissue. The reversion of PUFA metabolism by SGY may act through PPARα mediated Fads1 and Fads2 gene expression. The altered metabolites in liver showed intimate correlatship with modified genera. Conclusion Data indicated that SGY reshaped gut microbial structure and improved PUFA metabolism. These functions of SGY may alter hepatic lipid metabolism, conferring preventative effects against high-fat diet induced metabolic syndrome.
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