Published online Jul 7, 2015. doi: 10.3748/wjg.v21.i25.7621
Peer-review started: February 28, 2015
First decision: March 26, 2015
Revised: March 31, 2015
Accepted: May 21, 2015
Article in press: May 21, 2015
Published online: July 7, 2015
Irritable bowel syndrome (IBS) is a common gastrointestinal disorder, the pathophysiology of which is not completely known, although it has been shown that genetic/social learning factors, diet, intestinal microbiota, intestinal low-grade inflammation, and abnormal gastrointestinal endocrine cells play a major role. Studies of familial aggregation and on twins have confirmed the heritability of IBS. However, the proposed IBS risk genes are thus far nonvalidated hits rather than true predisposing factors. There is no convincing evidence that IBS patients suffer from food allergy/intolerance, with the effect exerted by diet seemingly caused by intake of poorly absorbed carbohydrates and fiber. Obesity is a possible comorbidity of IBS. Differences in the microbiota between IBS patients and healthy controls have been reported, but the association between IBS symptoms and specific bacterial species is uncertain. Low-grade inflammation appears to play a role in the pathophysiology of a major subset of IBS, namely postinfectious IBS. The density of intestinal endocrine cells is reduced in patients with IBS, possibly as a result of genetic factors, diet, intestinal microbiota, and low-grade inflammation interfering with the regulatory signals controlling the intestinal stem-cell clonogenic and differentiation activities. Furthermore, there is speculation that this decreased number of endocrine cells is responsible for the visceral hypersensitivity, disturbed gastrointestinal motility, and abnormal gut secretion seen in IBS patients.
Core tip: There are several factors that play a major role in the pathophysiology of irritable bowel syndrome (IBS). These factors are genetic disposition, diet, the intestinal microbiota, and mucosal low-grade inflammation. These factors are known to affect the gastrointestinal endocrine cells, with the densities of intestinal endocrine cells being reduced in IBS patients. The reduction in the gastrointestinal endocrine cells seems to be caused by abnormal clonogenic and differentiation activities of the intestinal stem cells. The abnormalities in the gastrointestinal endocrine cells can explain the visceral hypersensitivity, disturbed gastrointestinal motility, and abnormal gut secretion observed in IBS patients.