In some mice models, Interleukin-1 (IL-1), IL-6, and LPS all acutely increased plasma levels of GLP-1 [90], while the demonstration that Glp1r−/− mice exhibit gut microbial dysbiosis and markedly increased sensitivity to experimental colonic inflammation proved the importance of intestinal GLP-1 signaling for control of local inflammatory signals [91]. The gene discussed is GCG; the disease is inflammation.