Fructose-Sorbitol Malabsorption and Symptom Provocation in Irritable Bowel Syndrome: Relationship to Enteric Hypersensitivity and Dysmotility

Evans, P. R.; Piesse, C.; Bak, Young‐Tae; Kellow, John

doi:10.1080/00365529850172502

Cited by 37 publications

(5 citation statements)

References 6 publications

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“…A key observation in our study is that FOS consumption further intensified visceral hypersensitivity already present in mice subjected to WAS. This result is consistent with the clinical studies that demonstrated adverse effects of high FODMAP diet as an individual component or as an aggregate in exacerbating gastrointestinal symptoms in IBS[ 6 , 8 , 23 , 24 ]. Along the same vein, our findings are concordant with studies that demonstrated the efficacy of dietary restriction of FODMAP in improving gastrointestinal symptoms, such as abdominal pain, diarrhea, bloating, flatulence, and quality of life in IBS patients[ 7 , 9 , 25 ].…”

Section: Discussionsupporting

confidence: 91%

Fructo-oligosaccharide intensifies visceral hypersensitivity and intestinal inflammation in a stress-induced irritable bowel syndrome mouse model

Chen

et al. 2017

WJG

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AIMTo determine whether fructo-oligosaccharide (FOS) affects visceral sensitivity, inflammation, and production of intestinal short-chain fatty acids (SCFA) in an irritable bowel syndrome (IBS) mouse model.METHODSMice were randomly assigned to daily oral gavage of saline solution with or without FOS (8 g/kg body weight) for 14 d. Mice were further assigned to receive either daily one-hour water avoidance stress (WAS) or sham-WAS for the first 10 d. After 2 wk, visceral sensitivity was measured by abdominal withdrawal reflex in response to colorectal distension and mucosal inflammation was evaluated. Gas chromatography, real-time reverse transcription PCR, and immunohistochemistry assays were used to quantify cecal concentrations of SCFA, intestinal cytokine expression, and number of intestinal mast cells per high-power field (HPF), respectively.RESULTSMice subjected to WAS exhibited visceral hypersensitivity and low-grade inflammation. Among mice subjected to WAS, FOS increased visceral hypersensitivity and led to higher cecal concentrations of acetic acid (2.49 ± 0.63 mmol/L vs 1.49 ± 0.72 mmol/L, P < 0.05), propionic acid (0.48 ± 0.09 mmol/L vs 0.36 ± 0.05 mmol/L, P < 0.01), butyric acid (0.28 ± 0.09 mmol/L vs 0.19 ± 0.003 mmol/L, P < 0.05), as well as total SCFA (3.62 ± 0.87 mmol/L vs 2.27 ± 0.75 mmol/L, P < 0.01) compared to saline administration. FOS also increased ileal interleukin (IL)-23 mRNA (4.71 ± 4.16 vs 1.00 ± 0.99, P < 0.05) and colonic IL-1β mRNA (2.15 ± 1.68 vs 0.88 ± 0.53, P < 0.05) expressions as well as increased mean mast cell counts in the ileum (12.3 ± 2.6 per HPF vs 8.3 ± 3.6 per HPF, P < 0.05) and colon (6.3 ± 3.2 per HPF vs 3.4 ± 1.2 per HPF, P < 0.05) compared to saline administration in mice subjected to WAS. No difference in visceral sensitivity, intestinal inflammation, or cecal SCFA levels was detected with or without FOS administration in mice subjected to sham-WAS.CONCLUSIONFOS administration intensifies visceral hypersensitivity and gut inflammation in stress-induced IBS mice, but not in the control mice, and is also associated with increased intestinal SCFA production.

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Section: Discussionsupporting

confidence: 91%

Fructo-oligosaccharide intensifies visceral hypersensitivity and intestinal inflammation in a stress-induced irritable bowel syndrome mouse model

Chen

et al. 2017

WJG

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“…Jejunal motility was assessed using 24-h manometry and visceral sensation using a balloon distention model. Although both jejunal dysmotility and hypersensitivity were altered, the study did not find a significant association between dysmotility, carbohydrate malabsorption, and symptom provocation [58].…”

Section: Visceral Hypersensitivitycontrasting

confidence: 63%

“…Animal studies have demonstrated that hyperosmolar solutions of mannitol can stimulate duodenal motility, independent of changes in gastric inhibitory peptide or insulin [92,93]. A limited study on polyol consumption and gastrointestinal motility by Evans et al found no association between jejunal dysmotility, carbohydrate malabsorption, and symptom provocation in female patients with IBS [58].…”

Section: Motilitymentioning

confidence: 99%

The Role of the FODMAP Diet in IBS

Bertin,

Zanconato,

Crepaldi

et al. 2024

Nutrients

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The low FODMAP (fermentable oligosaccharide, disaccharide, monosaccharide, and polyol) diet is a beneficial therapeutic approach for patients with irritable bowel syndrome (IBS). However, how the low FODMAP diet works is still not completely understood. These mechanisms encompass not only traditionally known factors such as luminal distension induced by gas and water but also recent evidence on the role of FOMAPs in the modulation of visceral hypersensitivity, increases in intestinal permeability, the induction of microbiota changes, and the production of short-chain fatty acids (SCFAs), as well as metabolomics and alterations in motility. Although most of the supporting evidence is of low quality, recent trials have confirmed its effectiveness, even though the majority of the evidence pertains only to the restriction phase and its effectiveness in relieving abdominal bloating and pain. This review examines potential pathophysiological mechanisms and provides an overview of the existing evidence on the effectiveness of the low FODMAP diet across various IBS subtypes. Key considerations for its use include the challenges and disadvantages associated with its practical implementation, including the need for professional guidance, variations in individual responses, concerns related to microbiota, nutritional deficiencies, the development of constipation, the necessity of excluding an eating disorder before commencing the diet, and the scarcity of long-term data. Despite its recognized efficacy in symptom management, acknowledging these limitations becomes imperative for a nuanced comprehension of the role of a low FODMAP diet in managing IBS. By investigating its potential mechanisms and evidence across IBS subtypes and addressing emerging modulations alongside limitations, this review aims to serve as a valuable resource for healthcare practitioners, researchers, and patients navigating the intricate landscape of IBS.

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“…Moreover, a specific psychological profile has been related to the combination of abnormal jejunal postprandial motility and hypersensitivity in IBS 12 ) . Provocation of symptoms by fructose and sorbitol does not, however, appear related to visceral hypersensitivity, at least to hypersensitivity in the small intestine 24 ) . Although visceral hypersensitivity in patients with IBS may affect different levels of the small bowel, whether the ileum exhibits greater or lesser hypersensitivity than the jejunum in IBS is not established.…”

Section: Pathophysiological Mechanismsmentioning

confidence: 99%

Review : Pathophysiology and Management of Irritable Bowel Syndrome

Kellow

2001

Korean J Intern Med

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Fructose-Sorbitol Malabsorption and Symptom Provocation in Irritable Bowel Syndrome: Relationship to Enteric Hypersensitivity and Dysmotility

Abstract: Although carbohydrate malabsorption can provoke symptoms in some IBS patients, there is no consistent association between such a phenomenon and the presence of either jejunal hypersensitivity or dysmotility.

Cited by 37 publications

References 6 publications

Fructo-oligosaccharide intensifies visceral hypersensitivity and intestinal inflammation in a stress-induced irritable bowel syndrome mouse model

Fructo-oligosaccharide intensifies visceral hypersensitivity and intestinal inflammation in a stress-induced irritable bowel syndrome mouse model

The Role of the FODMAP Diet in IBS

Review : Pathophysiology and Management of Irritable Bowel Syndrome

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