Background:: Healthy colonic mucosa uses butyrate as the major energy source. In ulcerative colitis (UC) butyrate oxidation has been shown to be disturbed, but it remains unclear whether this is a primary defect. The aim of this study was to measure mucosal butyrate oxidation in UC (involved and noninvolved colon) and in pouchitis and to study the relationship with endoscopic as well as histological disease activity.
Methods:: Butyrate oxidation was measured in 73 UC patients, 22 pouchitis patients, and 112 controls (95 colon, 17 ileum) by incubating biopsies with 1 mM 14C‐labeled Na‐butyrate and measuring the released 14CO2.
Results:: Compared with that in normal colon, butyrate oxidation was significantly impaired in endoscopically active but not in quiescent disease or uninvolved colon segments. The severity of the metabolic defect was related to histological disease activity and decreased epithelial cell height. In active pouchitis, butyrate oxidation was significantly decreased compared with that in normal ileum and excluded pouches without inflammation. The histological pouchitis score correlated significantly with butyrate oxidation.
Conclusions:: Active UC and pouchitis show the same inflammation‐related metabolic defect. Our data suggest that the defect is a consequence of inflammation and that pouchitis is metabolically similar to active UC.
1Department of Gastrointestinal Research and Leuven Food Science and Nutrition Research Centre (LFoRCe), University Hospital Leuven, KU Leuven, Leuven, Belgium
2Department of Pathology, University Hospital, KU Leuven, Leuven, Belgium
Reprints: Paul Rutgeerts, Department of Gastroenterology, University Hospital Leuven, Herestraat 49, B‐3000 Leuven, Belgium
Received for publication August 14 2008; Accepted August 20 2008
Published online 22 October 2008 in Wiley InterScience (www.interscience.wiley.com).