EFFECTS OF ACARBOSE ON FECAL NUTRIENTS, COLONIC PH, AND SHORT-CHAIN FATTY-ACIDS AND RECTAL PROLIFERATIVE INDEXES

Acarbose, an ru-glycosidase inhibitor, treats diabetes mellitus by del aying the digestion and intestinal absorption of dietary carbohydrates . In effective doses, acarbose induces some passage of carbohydrates i nto the colon. The effect of such chronic carbohydrate transfer on col onic structure and function is unknown. We studied the effects of 1 ye ar of acarbose administration in diabetes mellitus on fecal energy, pr otein, and fat, including short-chain fatty acids (SCFA) output, fecal pH, and several metabolizing bacterial species. Changes in colonic hi stology and epithelial cell proliferation were investigated in rectal biopsies. Fecal macronutrient output was unaffected by acarbose, but p H decreased and total SCFA, butyrate, and acetate output were markedly greater. Breath hydrogen output increased after acarbose, but digoxin -metabolizing bacteria and diacylglycerol (DAG) production were unalte red. Compared with the control, acarbose did not induce hyperplasia or change rectal proliferation. However, total fecal SCFA and butyrate o utput correlated inversely with proliferation in the rectal upper cryp t-a biomarker of risk for colonic neoplasia. In conclusion, long-term acarbose administration does not adversely affect colonic function or fecal nutrient output. If increased fecal SCFA and butyrate reduces up per-crypt proliferation, then acarbose may reduce the risk of colonic neoplasia. Copyright (C) 1996 by W.B. Saunders Company