ILEAL AND COLONIC EPITHELIAL METABOLISM IN QUIESCENT ULCERATIVE-COLITIS - INCREASED GLUTAMINE-METABOLISM IN DISTAL COLON BUT NO DEFECT IN BUTYRATE METABOLISM

Previous studies have shown that butyrate is an important energy source for the distal colon, and that its metabolism may be defective in ulcerative colitis (UC). A similar metabolic defect in the ileum might account for the occurrence of 'pouchitis' in UC patients after colectomy. A method has been developed that allows the measurement of metabolism in ileocolonoscopic biopsy specimens, and this has been used to assess butyrate and glutamine metabolism in quiescent UC and controls. Preliminary experiments showed optimal metabolism of butyrate at 1 mmol/l. In controls glutamine metabolism was greater in the ascending (mean (SD)) (4-9 (3.2) nmol/h/pg protein) than in the descending colon (1.4 (0-7)) (p<0.05, Mann-Whitney U test), but butyrate metabolism was similar in the two regions (ascending 62.6 (44.2), descending 51.5 (32.0)). Consequently ratios of butyrate/glutamine metabolism were higher in the descending colon (20.6 (14.3)) than in the ascending colon (14.3 (9.6)) (p<0.05). In UC, rates of butyrate metabolism were similar in the ascending (92.5 (58.3) nmol/h/mug protein) and descending (93.3 (115)) colon, and these were not significantly different from controls. In UC, glutamine metabolism was similar in the ascending (6-2 (7.7) nmol/h/mug protein) and descending colon (7.8 (7.9)); the metabolism in the descending colon was significantly greater than in controls (p<0.01). Butyrate (135 (56) nmol/h/mug protein) and glutamine (24.1 (16.2)) metabolism in the ileum in UC, were not significantly different from control values (butyrate 111 (57), glutamine 15.5 (15.6)). These results confirm that there is regional variation of nutrient utilisation throughout the colon, but they do not support the hypothesis that UC is caused by a deficiency of butyrate metabolism.