PURPOSE: Fecal electrolytes and organic anion concentrations are altered in ulcerative colitis, presumably reflecting changes in colon epithelial transport. Information of mucosal absorption of butyrate in active ulcerative proctosigmoiditis is not available. METHODS: Dialysis bags containing 70 mmol/liter of butyrate in an isotonic electrolyte solution were placed in the rectum for 30 minutes. Net absorption or secretion rates of butyrate, lactate, and electrolytes were determined in the rectum of 12 patients with active ulcerative colitis (UC) and in 10 patients with quiescent UC and then compared with 10 healthy controls. RESULTS: Net flux rates demonstrated a considerable absorption of butyrate in patients with active inflammation of 7.5 +/- 0.4 mumol/cm2/h and quiescent colitis of 6.6 +/- 0.4 mumol/cm2/h, equal to absorption in healthy controls of 6.3 +/- 0.5 mumol/cm2/h, P = 0.12. Despite normal butyrate absorption, sodium absorption was compromised in active ulcerative colitis (11.5 +/- 1.4 mumol/cm2/h) compared with quiescent (15.4 +/- 1.0 mumol/cm2/h) and controls (18.7 +/- 0.8 mumol/cm2/h) (P = 0.0006). Mucosal secretion of L-lactate was minimal in both healthy controls and quiescent UC but significantly increased in patients with proctosigmoiditis (0.2 +/- 0.1 mumol/cm2/h, 0.2 +/- 0.1 mumol/cm2/h vs. 0.9 +/- 0.2 mumol/cm2/h; P = 0.0001). Appearance of D-lactate was negligible in all three groups. CONCLUSIONS: This study demonstrates that rectal butyrate absorption is normal in UC, and it follows that butyrate supplied in enemas can be expected to be absorbed. The inflamed colonic mucosa secretes L-lactate, and the increased fecal lactate concentrations can be explained by mucosal origin of lactate.
PURPOSE: Fecal electrolytes and organic anion concentrations are altered in ulcerative colitis, presumably reflecting changes in colon epithelial transport. Information of mucosal absorption of butyrate in active ulcerative proctosigmoiditis is not available. METHODS: Dialysis bags containing 70 mmol/liter of butyrate in an isotonic electrolyte solution were placed in the rectum for 30 minutes. Net absorption or secretion rates of butyrate, lactate, and electrolytes were determined in the rectum of 12 patients with active ulcerative colitis (UC) and in 10 patients with quiescent UC and then compared with 10 healthy controls. RESULTS: Net flux rates demonstrated a considerable absorption of butyrate in patients with active inflammation of 7.5 +/- 0.4 mumol/cm2/h and quiescent colitis of 6.6 +/- 0.4 mumol/cm2/h, equal to absorption in healthy controls of 6.3 +/- 0.5 mumol/cm2/h, P = 0.12. Despite normal butyrate absorption, sodium absorption was compromised in active ulcerative colitis (11.5 +/- 1.4 mumol/cm2/h) compared with quiescent (15.4 +/- 1.0 mumol/cm2/h) and controls (18.7 +/- 0.8 mumol/cm2/h) (P = 0.0006). Mucosal secretion of L-lactate was minimal in both healthy controls and quiescent UC but significantly increased in patients with proctosigmoiditis (0.2 +/- 0.1 mumol/cm2/h, 0.2 +/- 0.1 mumol/cm2/h vs. 0.9 +/- 0.2 mumol/cm2/h; P = 0.0001). Appearance of D-lactate was negligible in all three groups. CONCLUSIONS: This study demonstrates that rectal butyrate absorption is normal in UC, and it follows that butyrate supplied in enemas can be expected to be absorbed. The inflamed colonic mucosa secretes L-lactate, and the increased fecal lactate concentrations can be explained by mucosal origin of lactate.
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