Prevotella ‐Derived Butyrate Inhibits CD8 + T‐Cell Glycolysis via AKT / mTOR Signalling to Alleviate MASH

BACKGROUND AND AIMS: T-cell metabolism. METHODS: T-cell cultures were used to assess the effects of Prevotella and butyrate on glycolysis, PI3K/AKT/mTOR signalling and liver pathology. Metabolic activity was measured using ECAR, 2-NBDG uptake and lactate production; molecular changes were evaluated by qPCR, western blotting and flow cytometry. RESULTS: T cells, linking its metabolic effects to immune modulation. Notably, the combination of Prevotella with a glycolysis inhibitor did not further enhance its therapeutic efficacy compared with Prevotella alone, indicating that suppression of glycolysis is a major mechanism underlying Prevotella's protective effects. CONCLUSION: T cells via butyrate-dependent mechanisms, highlighting its potential as a microbial therapeutic candidate for MASH.