Butyrate improves testicular spermatogenic dysfunction induced by a high-fat diet

Obesity is closely associated with low male fertility and decreased sperm quality. Obesity is accompanied by an ecological imbalance in the gut microbiota, so it is of great significance to intervene in male infertility caused by obesity from the perspective of gut microbiota metabolites. This study aimed to evaluate the efficacy of butyrate in ameliorating obesity-induced spermatogenic dysfunction and to explore the potential molecular mechanisms.

This study explored the role of butyrate in recovering the dysfunctions of spermatogenesis caused by obesity by inducing an obese model of male mice with a high-fat diet (HFD). The effects of HFD and butyrate on testicular function were explored based on metabolomics.

The results of the study showed that HFD caused a decrease in sperm count, a decrease in sperm motility, and an increase in sperm malformation rate in mice. After adding butyrate to the HFD, the various sperm indicators of mice were significantly improved. Through the analysis of metabolomics data from mouse testes, this study found that an HFD significantly altered the metabolic status of mice testes, involving multiple metabolic pathways. However, after adding butyrate, some metabolic characteristics tended to be similar to those of normal diet mice, and the steroid biosynthesis and primary bile acid biosynthesis pathways were significantly improved.

This study clarified the effect of butyrate on improving sperm quality, providing experimental evidence for the treatment of obesity-induced abnormal spermatogenesis with butyrate.