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