Study of efficacy and mechanism of low FODMAPs diet on diarrhea-type irritable bowel syndrome based on a gut microbiota-dependent metabolite

Abstract

BACKGROUND The changes in gut microbiota-dependent metabolites can cause irritable bowel syndrome (IBS). It is important to investigate whether a diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) plays a therapeutic role in IBS treatment by affecting the production of phenylalanine (PHE), a gut microbiota-dependent metabolite. AIM To investigate the efficacy of a low FODMAPs diet in diarrhea-type irritable bowel syndrome (IBS-D) and its molecular mechanism for regulating GLP-1 secretion by affecting PHE, a gut microbiota-dependent metabolite. METHODS Thirty patients who met the Rome IV diagnostic criteria for IBS-D were enrolled and treated with a low FODMAPs diet for 4 wk. Thirty healthy volunteers served as baseline controls. The changes of clinical symptom scores, and serum PHE, GLP-1, and TNF-α, as well as IFN-γ before and after treatment were recorded. In in vitro experiment, different doses of PHE were added into NCI-H716 cells to observe the regulatory effect of PHE on GLP-1. RESULTS The clinical symptom scores after treatment in the IBS group were significantly lower than those before treatment (P < 0.0001 & P < 0.001). After treatment, the levels of PHE and GLP-1 increased (P < 0.05), but those of TNF-α and IFN-γ decreased significantly (P < 0.0001 & P < 0.001). No adverse reactions occurred in the IBS group. In in vitro experiment, GLP-1 expression levels were found to rise with increasing PHE concentrations, and 1 mmol/L PHE could significantly increase GLP-1 secretion. CONCLUSION Low FODMAPs diet improves the symptoms in IBS-D patients via mechanisms that may be related to the regulation of GLP-1 by affecting PHE and thereby inhibiting the secretion of pro-inflammatory cytokines.