Because GLP-1 modulates ACE2 expression in the cardiovascular system [29], we performed a series of studies to further elucidate the potential role of GLP-1 in regulating colon ACE2 expression in response to GPBAR1 agonism, and found that both the anti-inflammatory effects exerted by BAR501 in the TNBS model of colitis and positive regulation of Ace2 mRNA in the colon of these animals, were reversed by co-treating mice with exendin-3, a GLP-1-R antagonist [52]. The gene discussed is ACE2; the disease is colitis.