Gastroenterology

Gastroenterology

Volume 115, Issue 3, September 1998, Pages 584-590
Gastroenterology

Alimentary Tract
In vivo butyrate metabolism and colonic permeability in extensive ulcerative colitis,☆☆

https://doi.org/10.1016/S0016-5085(98)70137-4Get rights and content

Abstract

Background & Aims: Impaired short-chain fatty acid metabolism by the colonocyte has been suggested as a pathogenic factor in ulcerative colitis (UC). The aim of this study was to measure in vivo butyrate metabolism in UC and to correlate butyrate oxidation with colonic permeability. Methods: Butyrate oxidation was measured by means of a 14CO2-breath test after rectal instillation of 14C-butyrate. 51Cr-ethylenediaminetetraacetic acid (EDTA) was added to the enema, and the urinary % dose excretion of 51Cr-EDTA after 6 hours was a measure for permeability. Results: Patients with active extensive UC showed a significantly lower butyrate oxidation and increased colonic permeability in comparison to healthy controls. Butyrate oxidation correlated significantly negative with clinical activity. Oxidation of butyrate was not decreased in most patients with inactive extensive UC. In 3 patients with inactive disease and decreased oxidation, a relapse occurred within a few weeks after the test, whereas all patients with normal oxidation maintained their remission for at least 3 months. A significantly negative correlation existed between butyrate oxidation and colonic permeability. Conclusions: Patients with active extensive UC have a decreased colonic butyrate oxidation. However, the fact that remission is associated with normal oxidation suggests that UC mucosa is not intrinsically altered in butyrate oxidation, making this unlikely to be a primary defect in UC.

GASTROENTEROLOGY 1998;115:584-590

Section snippets

Subjects

All controls were healthy volunteers without gastrointestinal complaints who did not use medication (except oral contraceptives).

All patients had extensive UC reaching at least to the splenic flexure. All patients with active disease were hospitalized, and 22 of 25 patients with active UC received intravenous steroids, 7 in combination with immunosuppressants (Imuran [Burroughs Wellcome, Research Triangle Park, NC] or cyclosporine); 9 patients were administered mesalamine. Eleven patients were

Variable retention time

Figure 1 shows the mean (±SEM) 14CO2 % dose/h excretion between 0 and 6 hours in UC patients with active disease, in patients with inactive UC, and in healthy controls.

. % Dose per hour excretion of 14CO2 after rectal instillation of 14C-butyrate in patients with extensive UC and active disease (■, n = 15), patients with extensive UC and inactive disease (×, n = 11), and in healthy controls (□, n = 10). Means and SEM are given. *Significantly differed from active UC.

At each time point (except at

Discussion

Butyrate is one of the SCFAs that are end products of the colonic fermentation of mainly carbohydrates. It serves as a major source of energy for the colonocytes. An impaired production of butyrate, deficient uptake, or insufficient utilization might be involved in the pathogenesis of UC. A diminished5, 6, 7 as well as a normal8, 9 butyrate metabolism of colonocytes of UC patients have been noted in vitro. The technique of colonocyte preparation and incubation are of major importance and might

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    Address for requests for reprints to: Paul Rutgeerts, Department of Gastroenterology, University Hospital Leuven, Herestraat 49, B-3000 Leuven, Belgium. Fax: (32) 16-344419.

    ☆☆

    Supported by a grant from the Danone Institute (Clinical Research Grant in Human Nutrition).

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