Overview
- TMA, a metabolite produced from dietary choline, directly binds the immune kinase IRAK4 to curb fat-induced inflammation and restore insulin sensitivity in preclinical experiments.
- Evidence spans molecular target screening, human cell models, and mouse studies, with IRAK4 genetic deletion or pharmacologic inhibition mirroring TMA’s metabolic benefits.
- In mice fed high-fat diets, boosting choline intake raised circulating TMA roughly twentyfold and was linked with improved inflammatory and glycaemic readouts.
- A single TMA dose improved survival in a mouse model of LPS-induced sepsis, indicating broader anti-inflammatory effects beyond glucose control.
- The international team from Imperial College London, UCLouvain, and the University of Ottawa Heart Institute reports a translational path via IRAK4-directed drugs or diet–microbiome strategies, though human trials have yet to begin.