Researchers reported in Nature Communications that intestinal interleukin‑22 (IL‑22) elevates GLP‑1 production and improves glucose homeostasis in male mice, linking mucosal immunity to metabolic regulation. The study showed IL‑22 modulation altered enteroendocrine cell activity and systemic glycemic responses in obesity models. The mechanism suggests an immunometabolic axis that could be targeted for obesity‑related insulin resistance. Translational steps will require validation in diverse animal models and human tissues to evaluate safety, dosing, and the therapeutic window for immunomodulatory metabolic interventions.