Increasing Fecal Butyrate in Ulcerative Colitis Patients by Diet: Controlled Pilot Study *Claes Hallert, †Inger Björck, †Margareta Nyman, *Anneli Pousette, ‡Christer Grännö, and *Hans Svensson Departments of Internal Medicine, *Vrinnevi Hospital, Norrköping, and ‡Ryhov Hospital, Jönköping; and †Department of Applied Nutrition and Food Chemistry, Chemical Center, Lund University, Lund, Sweden Summary: Topical butyrate has been shown to be effective in the treatment of ulcerative colitis (UC). Butyrate is derived from colonic fermentation of dietary fiber, and our aim was to study whether UC patients could safely increase the fecal bu- tyrate level by dietary means. We enrolled 22 patients with quiescent UC (mean age, 44 years; 45% women; median time from last relapse, 1 year) in a controlled pilot trial lasting 3 months. The patients were instructed to add 60 g oat bran (corresponding to 20 g dietary fiber) to the daily diet, mainly as bread slices. Fecal short-chain fatty acids (SCFAs) including butyrate, disease activity, and gastrointestinal symptoms were recorded every 4 weeks. During the oat bran intervention the fecal butyrate concentration increased by 36% at 4 weeks (from 11 ± 2 (mean ± SEM) to 15 ± 2 mol/g feces) (p < 0.01). The mean butyrate concentration over the entire test period was 14 ±1 mol/g feces (p < 0.05). Remaining fecal SCFA levels were unchanged. No patient showed signs of colitis relapse. Unlike controls, the patients showed no increase in gastroin- testinal complaints during the trial. Yet patients reporting ab- dominal pain and reflux complaints at entry showed significant improvement at 12 weeks that returned to baseline 3 months later. This pilot study shows that patients with quiescent UC can safely take a diet rich in oat bran specifically to increase the fecal butyrate level. This may have clinical implications and warrants studies of the long-term benefits of using oat bran in the maintenance therapy in UC. Key words: -Glucans— Butyrate—Dietary fiber—Nutrition—Oat bran—Prebiotics— SCFA—Ulcerative colitis. Ulcerative colitis (UC) is a chronic disorder of un- known etiology. There is evidence to suggest that the central defect may reside in abnormalities in the function of the colonic epithelium. A hypothesis gaining increas- ing attraction (1,2) implicates impaired epithelial barrier function as a key event allowing influx of proinflamma- tory factors into the lamina propria. Much current interest addresses the role of the short- chain fatty acid (SCFA) butyrate in the maintenance of the colonic epithelium. Besides being the main fuel for the colonocyte, butyrate has a variety of biologic prop- erties that include trophic effects on crypts cells (3), in- crease in mucosal blood flow (4), reduction in mucosal permeability (5), and attenuation of destructive activities of neutrophils (6). Clinical trials have demonstrated that topical SCFAs mixture and butyrate monotherapy are effective in the treatment of diversion colitis, acute ra- diation proctitis, and distal UC (7–9). Considering that SCFAs are derived from bacterial degradation of indigestible carbohydrates in the colonic lumen, e.g. dietary fiber, the potential of regulating co- lonic butyrate production by dietary means is highly at- tractive. Contrary to the common belief that the roughage component of dietary fibers is traumatic to the colonic surface (2), we have previously shown in a placebo- controlled study that ispaghula husk supplementation is well tolerated and relieves gastrointestinal symptoms in quiescent UC patients (10). However, dietary fibers differ in the capacity to gen- erate butyric acid. A high proportion of butyric acid has been observed with barley -glucans in the rat hindgut (11). This prompted us to study whether it is feasible and Received September 25, 2001; accepted October 29, 2002. Address correspondence to Associate Professor Claes Hallert, B-HoS, 581 91 Linköping, Sweden. E-mail: Claes.Hallert@lio.se Inflammatory Bowel Diseases 9(2):116–121 © 2003 Crohn’s & Colitis Foundation of America, Inc. 116