While HO-1 activity is associated with obesity, metabolic syndrome, and even cardiovascular diseases, in the GI tract, HO-1 is shown to be transcriptionally implicated in ischemia-reperfusion, indomethacin-induced damage, lipopolysaccharide-associated sepsis, pancreatitis, and inflammatory bowel disease, indicating that the activation of HO-1 may act as an endogenous defensive mechanism to reduce the inflammation and tissue injury in the GI tract [37,40,41]. This evidence concerns the gene HMOX1 and obesity due to melanocortin 4 receptor deficiency.