Overview
- Researchers report that trimethylamine produced by gut bacteria from choline-rich foods binds IRAK4 and blunts inflammation triggered by high-fat diets.
- Human cell assays, mouse experiments, and molecular target screening showed direct IRAK4 inhibition with improved insulin sensitivity and better glycemic control.
- In mouse models, TMA also prevented death from sepsis by dampening overwhelming inflammatory responses.
- Eliminating IRAK4 genetically or blocking it with drugs reproduced TMA’s benefits, identifying a practical therapeutic target for insulin resistance.
- The international study led by teams at Imperial College London, UCLouvain, CNRS, and the University of Ottawa Heart Institute remains preclinical pending further validation and clinical testing.