What question did this study set out to answer?

To investigate how gut microbiota affects spermatogenesis in Ggt1-deficient mice through specific signaling pathways.

April 23, 2026Open Access

Gut microbiota induces dysspermatogenesis via microbial-derived phenylacetylglycine in Ggt1-deficient mice

Key Points

To investigate how gut microbiota affects spermatogenesis in Ggt1-deficient mice through specific signaling pathways.
Analyzed gut microbiota dysbiosis due to Ggt1 deletion.
Examined β2AR-STAT3-SOCS3-STAT5B-Klk1bs signaling pathway activation.
Evaluated the effect of microbial-derived phenylacetylglycine (PAGly) on spermatogenesis.
Ggt1 deficiency led to significant dysbiosis in gut microbiota.
PAGly induced β2AR activation, promoting STAT3 phosphorylation and SOCS3 expression.
Suppression of STAT5B activity resulted in decreased Klk1bs transcription, disrupting spermatogenesis.

Abstract

Ggt1 deletion-induced gut microbiota dysbiosis disrupts spermatogenesis via β2AR-STAT3-SOCS3-STAT5B-Klk1bs signaling pathway. Specifically, PAGly-induced β2AR activation promotes STAT3 phosphorylation, which induces SOCS3 to suppress p-STAT5B dependent Klk1bs transcription. This mechanism underscores the critical role of gut-derived metabolites in regulating testicular function and identifies potential targets for microbiota-modulated male infertility. Video Abstract.

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Cite This Study

Tang et al. (Tue,) studied this question.

synapsesocial.com/papers/69e9b71b85696592c86eb232 https://doi.org/https://doi.org/10.1186/s40168-026-02401-0

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