TY - JOUR
T1 - Probiotic Bifidobacterium reduces serum TMAO in unstable angina patients via the gut to liver to heart axis
AU - Zhou, Zhihong
AU - Sun, Lizhe
AU - Zhou, Wei
AU - Gao, Wen
AU - Yuan, Xiao
AU - Zhou, Huijuan
AU - Ren, Yuzhen
AU - Li, Bihua
AU - Wu, Yue
AU - She, Jianqing
N1 - Publisher Copyright:
© 2025 The Third Affiliated Hospital of Sun Yat-sen University
PY - 2025/3
Y1 - 2025/3
N2 - Background and aims: Studies indicate that the gut microbiota and its metabolites are involved in the progression of cardiovascular diseases, and enterohepatic circulation plays an important role in this progression. This study aims to identify potential probiotics for the treatment of unstable angina (UA) and elucidate their mechanisms of action. Methods: Initially, the gut microbiota from patients with UA and control was analyzed. To directly assess the effects of Bifidobacterium supplementation, 10 patients with UA were enrolled and administered Bifidobacterium (630 mg per intake twice a day for 1 month). The fecal metagenome, serum trimethylamine N-oxide (TMAO) levels, and other laboratory parameters were evaluated before and after Bifidobacterium supplementation. Results: After supplementing with Bifidobacterium for 1 month, there were statistically significant differences (P < 0.05) in TMAO, aspartate aminotransferase, total cholesterol, and low-density lipoprotein compared to before. Additionally, the abundance of Bifidobacterium longum increased significantly, although the overall abundance of Bifidobacterium did not reach statistical significance. The gut microbiota, metabolites, and gut-liver axis are involved in the progression of UA, and potential mechanisms should be further studied. Conclusions: Metagenomic analysis demonstrated a reduced abundance of Bifidobacterium in patients with UA. Supplementation with Bifidobacterium restored gut dysbiosis and decreased circulating TMAO levels in patients with UA. This study provides evidence that Bifidobacterium may exert cardiovascular-protective effects through the gut–liver–heart axis. Clinical trial number: ChiCTR2400093946.
AB - Background and aims: Studies indicate that the gut microbiota and its metabolites are involved in the progression of cardiovascular diseases, and enterohepatic circulation plays an important role in this progression. This study aims to identify potential probiotics for the treatment of unstable angina (UA) and elucidate their mechanisms of action. Methods: Initially, the gut microbiota from patients with UA and control was analyzed. To directly assess the effects of Bifidobacterium supplementation, 10 patients with UA were enrolled and administered Bifidobacterium (630 mg per intake twice a day for 1 month). The fecal metagenome, serum trimethylamine N-oxide (TMAO) levels, and other laboratory parameters were evaluated before and after Bifidobacterium supplementation. Results: After supplementing with Bifidobacterium for 1 month, there were statistically significant differences (P < 0.05) in TMAO, aspartate aminotransferase, total cholesterol, and low-density lipoprotein compared to before. Additionally, the abundance of Bifidobacterium longum increased significantly, although the overall abundance of Bifidobacterium did not reach statistical significance. The gut microbiota, metabolites, and gut-liver axis are involved in the progression of UA, and potential mechanisms should be further studied. Conclusions: Metagenomic analysis demonstrated a reduced abundance of Bifidobacterium in patients with UA. Supplementation with Bifidobacterium restored gut dysbiosis and decreased circulating TMAO levels in patients with UA. This study provides evidence that Bifidobacterium may exert cardiovascular-protective effects through the gut–liver–heart axis. Clinical trial number: ChiCTR2400093946.
KW - Bifidobacterium
KW - Gut–liver–heart axis
KW - Trimethylamine N-oxide (TMAO)
KW - Unstable angina pectoris
UR - https://www.scopus.com/pages/publications/105001078097
U2 - 10.1016/j.livres.2025.02.001
DO - 10.1016/j.livres.2025.02.001
M3 - 文章
AN - SCOPUS:105001078097
SN - 2096-2878
VL - 9
SP - 57
EP - 65
JO - Liver Research
JF - Liver Research
IS - 1
ER -