Intestinal bacterial colonization may protect against atherosclerosis!

Release date:

2023-09-20

Recently, research conducted by Liu Hongwei, Liu Shuangjiang, and colleagues at the Institute of Microbiology, Chinese Academy of Sciences, has indicated that the human gut microbiota plays a pivotal role in cardiovascular diseases. Targeted modulation of the gut microbiome holds significant therapeutic potential for managing cardiovascular conditions.
　　
　　Researchers found that a terpenoid compound significantly ameliorated atherosclerotic symptoms in mice. Upon investigating the underlying mechanisms, they discovered that, following administration of this compound, the abundance of the core gut bacterium Parabacteroides distasonis increased 420-fold.
　　
　　Furthermore, an analysis of 405 patients with atherosclerosis from China and 647 patients with cardiovascular disease from Europe demonstrated that the abundance of Faecalibacterium prausnitzii in the gut was significantly negatively correlated with cardiovascular disease.
　　
　　Researchers further developed a model and found that, in mice with atherosclerosis, colonization with the human-derived bacterium Parabacteroides distasonis significantly alleviated atherosclerotic symptoms.
　　
　　The researchers further conducted targeted metabolomic analysis and found that, following colonization by Faecalibacterium prausnitzii, the levels of branched-chain short-chain fatty acids in mouse feces were significantly elevated, while the concentrations of branched-chain amino acids in both feces and blood were markedly reduced.
　　
　　Moreover, elevated blood levels of branched-chain amino acids have been shown to be closely associated with the onset and progression of insulin resistance, fatty liver disease, and cardiovascular diseases.
　　
　　Genomic analysis and in vitro fermentation experiments have demonstrated that Faecalibacterium prausnitzii can degrade branched-chain amino acids into branched-chain short-chain fatty acids. Following the knockout of porA, a key gene involved in the degradation of branched-chain amino acids in Faecalibacterium prausnitzii, its anti-atherosclerotic effects were abolished.
　　
　　Medical Information Network has learned that research has also demonstrated that Faecalibacterium prausnitzii can reduce plasma branched-chain amino acid levels by promoting the catabolism of these amino acids in the gut, thereby inhibiting the activation of the mTORC1 signaling pathway in macrophages within atherosclerotic plaques and exerting an anti‑atherosclerotic effect.
　　
　　
　　
　　Reposted from: “Chinese Journal of Circulation”