A Nature Communications study found that intestinal interleukin‑22 increases production of GLP‑1, improving glucose homeostasis in male mice and reversing obesity‑induced insulin resistance. Authors propose IL‑22‑mediated modulation of enteroendocrine cells as a pathway to enhance incretin responses. Results remain preclinical, but the pathway suggests an alternative route to GLP‑1 augmentation that could complement or inspire new therapies for type 2 diabetes and metabolic disease if translatable to humans.