Plasma glucagon-like peptide 1 and peptide YY levels are not altered in symptomatic fructose-sorbitol malabsorption

摘要

Background: Self-reported food hypersensitivity remains unexplained in most cases.Abdominal symptoms, typically consistent with the irritable bowel syndrome (IBS),are common in patients with such unexplained, self-reported food hypersensitivity.The etiology is obscure.Aim: The overall objective of the present study was to investigate possiblemechanisms of postprandial abdominal symptom generation. A main purpose was toexplore whether and how ingestion of low-digestible carbohydrates act as abdominalsymptom triggers in patients with unexplained, self-reported food hypersensitivity.Main results: The findings can be summarized as follows:In study I, fructose-sorbitol malabsorption evoked more symptoms in patients withunexplained, self-reported food hypersensitivity than in healthy controls. Alterationsin intestinal gas production and secretion of so-called ileal brake hormones(glucagon-like peptide 1 (GLP-1) and peptide YY (PYY)) could not be demonstrated.In study II, serum levels of chromogranin A (CgA) were found to be lower in patientswith unexplained, self-reported food hypersensitivity than in healthy controls.In study III, lactulose malabsorption evoked more symptoms in patients withunexplained, self-reported food hypersensitivity than in healthy controls. Thesymptoms could not be fully explained by symptom anticipation, because lactuloseinduced more symptoms than placebo (glucose). Associated alterations in intestinalgas production and rectal levels of prostaglandin E2 (PGE2) and microbialfermentation products could not be demonstrated.In study IV, mechanisms of diarrhoea in a mouse model of food allergy wereinvestigated. Changes within the jejunum were demonstrated in the food allergicmice, with development of muscular hypocontractility, increased levels of cytokinesIL-4 and IL-6 and high numbers of mast cells. In study V, fecal levels of short-chain fatty acids (SCFA) were investigated, and theprofile was different between patients with unexplained, self-reported foodhypersensitivity and healthy controls. Increased proportions of butyric acid weredemonstrated in the patient group, particularly in individuals with severe symptoms.Conclusion: Taken together, the results suggest that intolerance to low-digestiblecarbohydrates plays an important role in abdominal symptom generation in patientswith unexplained, self-reported food hypersensitivity. Disturbances of intestinalmotility may contribute to gastrointestinal symptom development by increasing theamount of malabsorbed carbohydrates. Altered intestinal fermentation is a potentialcause of the patients’ unexplained symptoms.