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Clostridium butyricum reduce lipogenesis through bacterial wall components and butyrate.

Abstract：

:Intervention strategies for obesity are global issues that require immediate attention. The objective of this study was to assess the possibility that Clostridium butyricum and its potential components could reduce lipogenesis. Co-culture experiments of Caco-2 cells and 1 × 10(6), 1 × 10(7), and 1 × 10(8) CFU/ml of C. butyricum were set up to monitor the cytotoxicity of C. butyricum and the changes of angiopoietin-like protein 4 (ANGPTL4) mRNA expression. It was found that cell viability was not affected by C. butyricum, and ANGPTL4 mRNA expression in Caco-2 cells was highly induced by 1 × 10(7) CFU/ml of C. butyricum. Co-culture experiment of Caco-2 cells and potential components of C. butyricum were set up to monitor any ensuing alteration in ANGPTL4. It was observed that bacterial wall components and potentially secreted factors from C. butyricum could induce ANGPTL4 mRNA expression and protein secretion. To determine whether butyrate could affect the ANGPTL4 production in Caco-2 cells, the role of monocarboxylate transporter 1 (MCT1) in mediating potentially secreted factors from C. butyricum-induced ANGPTL4 production in Caco-2 cells and the effect of 0.1 mM of butyrate on ANGPTL4 production in Caco-2 cells were investigated. It is confirmed that butyrate was the factor secreted by C. butyricum to stimulate ANGPTL4 production. Besides, the soluble factors secreted by live C. butyricum-Caco-2 cells interaction, bacterial wall components-Caco-2 cells interaction, and the main metabolites butyrate-Caco-2 cells interaction reduced lipogenic gene expression in HepG2 cells. In conclusion, 1 × 10(7) CFU/ml of C. butyricum could reduce lipogenesis through the bacterial wall components and the metabolites such as butyrate.

journal_name

Appl Microbiol Biotechnol

journal_title

Applied microbiology and biotechnology

authors

Zhao X,Guo Y,Liu H,Gao J,Nie W

doi

10.1007/s00253-014-5829-x

subject

Has Abstract

pub_date

2014-09-01 00:00:00

pages

7549-57

issue

17

eissn

0175-7598

issn

1432-0614

journal_volume

98

pub_type

杂志文章

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