Impairment of spermatogenesis and sperm motility by the high-fat diet-induced dysbiosis of gut microbes.
Level 5 - mechanism / opinion, no new human data
Preclinical animal fecal microbiota transplantation experiment combined with a cross-sectional human correlational cohort
PubMed 31900292 · doi:10.1136/gutjnl-2019-319127
What was done
Fecal microbiota from high-fat diet (HFD) or normal diet (ND) male mice was transplanted into recipient mice maintained on a normal diet. Researchers evaluated gut microbiota composition, sperm count, sperm motility, intestinal immune cell infiltration, epididymal pro-inflammatory cytokines, and testicular gene expression via RNA sequencing. Additionally, fecal, semen, and blood samples from human clinical subjects were analyzed to assess correlations between gut microbiota composition, blood endotoxin levels, and sperm quality parameters.
What was found
Recipient mice receiving HFD fecal microbiota transplantation (HFD-FMT) exhibited significant decreases in spermatogenesis and sperm motility compared to ND-FMT controls. HFD-FMT mice demonstrated increased abundance of Bacteroides and Prevotella, higher metabolic endotoxemia, intestinal infiltration of T cells and macrophages, elevated epididymal pro-inflammatory cytokines, and down-regulated testicular genes related to meiosis and mitochondrial function. In human samples, Bacteroides-Prevotella abundance correlated negatively with sperm motility, while Bacteroides abundance correlated positively with circulating endotoxin levels. The abstract reported no specific numerical values, confidence intervals, or sample sizes.
Why it matters
This study provides mechanistic evidence that diet-induced gut dysbiosis directly contributes to impaired spermatogenesis and sperm motility through endotoxemia and localized genital tract inflammation. It highlights a potential gut-testis axis linking metabolic disruption to male subfertility.
Limits
Causal mechanisms were demonstrated only in mice, whereas human data were purely correlational. Sample sizes for both mouse groups and human participants were not reported in the abstract. Confounding lifestyle and dietary factors in the human cohort were not detailed.
Cited by
- supports Lipopolysaccharide produced by gut dysbiosis can leak into circulation and trigger inflammation at the epididymis where sperm mature.