Prevotella ‐Derived Butyrate Inhibits CD8 + T‐Cell Glycolysis via AKT / mTOR Signalling to Alleviate MASH | Synapse
March 26, 2026
Prevotella ‐Derived Butyrate Inhibits CD8 + T‐Cell Glycolysis via AKT / mTOR Signalling to Alleviate MASH
Puntos clave
The aim is to explore how Prevotella-derived butyrate affects CD8+ T-cell function in the context of MASH.
Examined the role of Prevotella and butyrate in CD8+ T cells
Analyzed the PI3K/AKT/mTOR pathway activity
Assessed glycolysis levels in T cells
Butyrate from Prevotella significantly downregulated glycolysis in CD8+ T cells
PI3K/AKT/mTOR signaling was inhibited, correlating with reduced glycolysis
The findings indicate a potential therapeutic role for butyrate in managing MASH
Resumen
Prevotella mitigates MASH by downregulating the PI3K/AKT/mTOR-glycolysis axis in CD8+ T cells via butyrate-dependent mechanisms, highlighting its potential as a microbial therapeutic candidate for MASH.