Irritable bowel syndrome: Epidemiology, overlap disorders, pathophysiology and treatment

Figure 4 Pathology of irritable bowel syndrome in the intestinal. Food and microbial metabolism stimulate the gut's endocrine cells to release hormones and neurotransmitters, leading to visceral pain and reducing gastrointestinal motility. Apelin, corticotropin-releasing factor, and Toll-like receptor 4-proinflammatory cytokine signaling lead to visceral hypersensitivity and disruption of the gut barrier. The concentrations of hydrogen and methane are related to abnormal oroanal transit time (OATT), and a more rapid OATT was associated with a higher severity of abdominal discomfort, rumbling, and nausea. Decreasing miR-199 caused visceral hypersensitivity and augmented visceral pain in patients with irritable bowel syndrome (IBS) through translational upregulation of TRPV1. Colonic mucosal protein expression and faecal bile acids were correlated with the symptom severity of IBS-D patients. CRF: Corticotropin-releasing factor; TLR4: Toll-like receptor 4.