Published online Nov 21, 2019. doi: 10.3748/wjg.v25.i43.6416
Peer-review started: September 19, 2019
First decision: October 14, 2019
Revised: October 19, 2019
Accepted: November 1, 2019
Article in press: November 1, 2019
Published online: November 21, 2019
Processing time: 62 Days and 14.8 Hours
Irritable bowel syndrome (IBS) is a highly prevalent functional bowel disorder and the pathogenesis is complicated. Fecal metabolites are associated with gut visceral sensitivity, mucosal immune function and intestinal barrier function, all of which have critical roles in the pathogenesis of IBS.
A few articles reported that patients diagnosed with IBS had metabolite compositions that were different from those of healthy controls. However, the role of metabolites in IBS pathophysiology is unclear. The study of fecal metabolites might add insight to investigate IBS.
IBS with predominant diarrhea (IBS-D) is the major subtype of IBS. The aims of this study were to compare fecal metabolites in subjects with or without IBS-D and to explore the associations of metabolites with clinical and experimental parameters.
Participants underwent clinical and psychological assessments, including the IBS Symptom Severity System, an Italian modified version of the Bowel Disease Questionnaire, the Bristol Stool Form Scale, the Hospital Anxiety and Depression Scale, and the VSI, along with visceral sensitivity testing. Fecal metabolites were measured by targeted metabolomics approaches. Correlation analyses between these parameters were performed. SPSS (IBM-SPSS Statistics, Chicago, IL, United States) version 21.0 was used for statistical analysis.
The patients presented with more psychological symptoms and increased visceral hypersensitivity compared with the controls. In fecal metabolites, His, Ala, Tyr, Phe, and Trp were decreased in IBS-D patients, but isohexanoate was increased. Abdominal pain or visceral hypersensitivity was correlated with isovalerate, valerate and isohexanoate. Furthermore, a significant correlation was observed between metabolites and symptom severity.
This study presented evidence that metabolite compositions were different in subjects with or without IBS-D and some metabolites might be one of the origins or exacerbating factors of symptoms via increasing visceral sensitivity. This study also demonstrated a possible potential biomarker panel of symptom severity. The authors believe that this study provides some clues for IBS-D pathogenesis and for the search for biomarkers in symptom severity.
This preliminary study investigated the possible role of fecal metabolites in IBS pathophysiology. In the future, we will focus on the following aspects. First, as the present study did not standardize diet and could not make cause and effect inferences, conclusions need to be further verified by additional well-designed clinical and basic studies. Second, the present study focused on IBS-D patients, and the conclusions may not be generalized to other IBS subtypes. We will investigate the role of fecal metabolites in pathophysiology of other IBS subtypes in future studies.