Abstract
Supplementation of probiotics is a promising gut microbiota-targeted therapeutic method for hyperlipidemia and atherosclerosis. However, the selection of probiotic candidate strains is still empirical. Here, we obtained a human-derived strain, Lactobacillus mucosae A1, which was shown by metagenomic analysis to be promoted by a high-fiber diet and associated with the amelioration of host hyperlipidemia, and validated its effect on treating hyperlipidemia and atherosclerosis as well as changing structure of gut microbiota in ApoE-/- mice on a Western diet. L. mucosae A1 attenuated the severe lipid accumulation in serum, liver and aortic sinus of ApoE-/- mice on a Western diet, while it also reduced the serum lipopolysaccharide-binding protein content of mice, reflecting the improved metabolic endotoxemia. In addition, L. mucosae A1 shifted the gut microbiota structure of ApoE-/- mice on a Western diet, including recovering a few members of gut microbiota enhanced by the Western diet. This study not only suggests the potential of L. mucosae A1 to be a probiotic in the treatment of hyperlipidemia and atherosclerosis, but also highlights the advantage of such function-based rather than taxonomy-based strategies for the selection of candidate strains for the next generation probiotics.
Highlights
Hyperlipidemia, which results from an imbalanced lipid metabolism, is considered as a strong risk issue for the development of atherosclerosis [1,2]
After blasting against the 16S rRNA sequences database of bacteria and archaea on the national center for biotechnology information (NCBI), we found that the 16S rRNA gene of the A1 strain had the highest similarity with L. mucosae LM1 (99.87%) and the A1 strain belonged to the species L. mucosae (Figure 1B)
Administration of L. mucosae A1 reduced the effects of the Western diet on liver, resulting in significantly lower weight, triglyceride content and steatosis of liver (Figure 2E–G). These results demonstrated the ability of L. mucosae A1 to mitigate abnormal lipid metabolism in Western diet-fed ApoE-/- mice
Summary
Hyperlipidemia, which results from an imbalanced lipid metabolism, is considered as a strong risk issue for the development of atherosclerosis [1,2]. Studies have revealed several mechanisms of gut microbiota participating in the lipid metabolism of the host, such as the metabolism of bile acids [10], the production of short chain fatty acids (SCFAs) [11], and the translocation of lipopolysaccharide (LPS) over the gut barrier [12]. Gut microbiota can modulate the generation of TMAO through the pathway for TMA production [13], and through altering FMO3 (the most active member in metabolizing TMA to TMAO of FMO family in the liver) expression via processing bile acids [14]. Gut microbiota may serve a promising therapeutic target for managing hyperlipidemia and atherosclerosis [15]
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