Bifidobacterium animalis subsp.lactis F1-7/Pet Probiotics powder

Products customized are acceptable.

Potency: 10B CFU/g, 50B CFU/g, 100B CFU/g, 200B CFU/g, 300B CFU/g, 400B CFU/g, 500B CFU/g 

Shelf life: 24 months

Storage conditions: Stored at -18℃or below

The findings of a 2020 study titled "Reduction of intestinal trimethylamine by probiotics ameliorated lipid metabolic disorders associated with atherosclerosis." The research investigated the effects of probiotics with trimethylamine (TMA) degradation capabilities on TMAO and related lipid metabolism in mice.

Background

* Atherosclerosis (AS) is a primary pathological basis for cardiovascular diseases.

* Trimethylamine N-oxide (TMAO) has been shown to independently predict the risk of major adverse cardiac events.

* Certain gut microbiota can convert dietary choline, betaine, and carnitine into TMA. TMA is oxidized in the liver by flavin monooxygenase 3 (FMO3) to produce TMAO.

* Excessive TMAO in the body reduces bile acid content, leading to reduced reverse cholesterol transport, thereby affecting blood lipid metabolism.

* Reducing circulating TMAO can improve AS.

Methods

* Strain Screening: Five strains capable of effectively degrading TMA were screened from 10 probiotic strains with lipid-lowering capabilities.

* Animal Experiments: Mice were divided into a normal group, a high-choline group, and six probiotic intervention groups for a 6-week intervention.

* Indicator Detection: The content of TMA and TMAO in the cecum and serum, as well as the expression levels of the FMO3 and CYP7A1 genes in the liver, were detected.

* Histopathological Analysis: The pathological morphology of liver tissue was observed.

* Probiotic Colonization Experiment: Fluorescence labeling technology was used to detect the colonization of probiotics in the mouse intestine.

Results

* In vitro TMA Degradation: Among the 10 probiotic strains, five could effectively degrade TMA in vitro, namely F1-3-2, F1-7, F3-2, 1F-6, and NFGSQ.

* Cecal TMA Content: Compared with the high-choline group, the cecal TMA content of mice in the F1-3-2, F3-2, NFGSQ, and LGG groups was significantly reduced.

* Serum TMA and TMAO Content: Compared with the high-choline group, the serum TMA and TMAO content of mice in the F1-3-2, F3-2, NFGSQ, and LGG groups were significantly reduced.

* FMO3 Expression: Neither high-choline diet nor probiotic intervention significantly affected the expression level of the FMO3 gene in the liver.

* Blood Lipid Levels: Compared with the high-choline group, the serum total cholesterol (TC) and triglyceride (TG) levels of mice in the F1-3-2 group were significantly reduced, and liver fat accumulation was improved.

* Hepatic Lipid Accumulation: Compared with the high-choline group, the degree of hepatic steatosis in mice in the F1-3-2, F1-7, and LGG groups was significantly improved.

* Gene Expression: Compared with the high-choline group, the expression levels of the cholesterol 7-α-hydroxylase (CYP7A1) gene in the liver of mice in the F1-3-2, F1-7, and LGG groups were significantly increased, and the expression of the farnesoid X receptor (FXR) gene in the intestine was downregulated.

* Intestinal Colonization: The F1-3-2 strain could colonize in the cecum of mice.

Conclusion

* Probiotics (F1-3-2, F1-7, F3-2) can effectively reduce the content of TMA and TMAO in the cecum and serum of mice, improve lipid metabolic disorders, and reduce hepatic lipid accumulation. The F1-3-2 strain performed the best, effectively colonizing the mouse intestine and improving lipid metabolism through multiple pathways, making it an ideal candidate strain for developing probiotic preparations for the prevention and treatment of atherosclerosis.