A 2025 study in Signal Transduction and Targeted Therapy reveals that high fructose consumption directly reprograms CD4+ T cells, promoting inflammatory Th1 and Th17 cell generation through mTORC1 activation via glutamine metabolism. Reactive oxygen species (ROS)-driven TGF-β activation also contributes to Th17 expansion. In mouse models, high fructose intake worsened colitis without raising blood glucose or body weight. Crucially, the diabetes drug metformin reversed these effects by suppressing mTORC1 and reducing ROS-mediated TGF-β activation, pointing to a novel therapeutic strategy for diet-induced immune dysregulation.
