Bifidobacterium animalis subsp. lactis A12 prevents obesityassociated dyslipidemia by modulating gut microbiota-derived short-chain fatty acid production and energy metabolism in high-fat diet-fed mice

Abstract

Background: Bifidobacterium lactis A12 (B. lactis A12) has been shown to have the potential to prevent obesity. However, the mechanisms by which it affects the control of energy metabolism have not been fully elucidated. Objective: The present work aimed to clarify the mechanisms by that B. lactis A12 has an effect on the management of energy metabolism. Design: Three- to five-week-old male C57BL/6J mice were randomly divided into five groups, 15 mice for each group. Low-fat diet (LFD) group and high-fat diet (HFD) group were fed with phosphate-buffered saline (PBS) on a daily basis. Cell-free supernatant (CFS), A12, and B. lactis BB12 (BB12) groups were fed with daily probiotics for 10 weeks (1 × 109 CFU of every strain). Results: The results showed that A12 effectively alleviated relieved weight gain and dyslipidemia, inhibited liver adipose accumulation, and improved leptin resistance in HFD-fed mice (p < 0.05). The anti-obesity effects of B. lactis A12 were closely related to the assembly of short-chain fatty acids (SCFAs), SCFA-downstream receptors, and glucagon-like peptide-1 (GLP-1) secretion. Additionally, high-throughput sequencing of the 16S rRNA showed that B. lactis A12 supplementation reversed HFD-induced gut microbiota dysbiosis, which was possible related to the augmented abundance of SCFA-producing bacterium and a minimized ratio of Bacteroidetes to Firmicutes in mice. Conclusions: B. lactis A12 prevents obesity in some pathways, including the downregulation of sterol regulatory element binding protein-1 mRNA levels in the liver, modulation of the structure of gut microbiota in a gut microbiota-dependent manner, and the upregulation of the SCFA-producing bacteria-related G protein-coupled receptor 43 pathway.