1. Beneficial effects of Akkermansia muciniphila on benign prostatic hyperplasia and metabolic syndrome.
- Author
-
Wu S, Yin X, Yang P, Gong B, and Wang Z
- Abstract
Benign prostatic hyperplasia (BPH) is a prevalent condition associated with male lower urinary tract symptoms (LUTS) and is influenced by metabolic syndrome (MetS) and gut microbiota. Akkermansia muciniphila (AKK) is a gut commensal that has emerged as a potential modulator of metabolic health and inflammatory conditions. This study investigated the correlation between Akkermansia abundance and BPH severity and metabolic indices in fecal and serum samples from BPH patients and healthy donors using 16S rRNA sequencing and metabolic profiling. A testosterone-induced BPH mouse model was used to evaluate the effects of AKK administration on BPH severity and metabolic indices. Altered gut microbiota diversity was observed in BPH patients, with a significant reduction in Akkermansia abundance. Akkermansia abundance was negatively correlated with BPH symptom score, serum lipopolysaccharides (LPS), body mass index (BMI), blood glucose, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C). AKK administration in BPH mice resulted in histopathological improvements, reduced prostate index, and amelioration of glandular hyperplasia. Although changes in blood glucose, TC, and LDL-C levels post-AKK supplementation were not statistically significant, a trend toward improvement was noted. Additionally, AKK administration led to a reduction in systemic inflammation markers and restoration of intestinal barrier integrity. In conclusion, AKK might modulate the gut microbiota-prostate axis and MetS. AKK's influence on systemic inflammation and gut barrier function suggests its therapeutic promise in managing BPH and associated metabolic disorders. These findings pave the way for novel microbiota-targeted therapies in the treatment of BPH and MetS., Competing Interests: Declaration of Competing Interest None, (Copyright © 2025. Published by Elsevier Inc.)
- Published
- 2025
- Full Text
- View/download PDF