SMALL-INTESTINAL MALABSORPTION AND COLONIC FERMENTATION OF RESISTANT STARCH AND RESISTANT PEPTIDES TO SHORT-CHAIN FATTY-ACIDS

Some starch and protein, as well as fiber, remains unabsorbed in the small intestine and is degraded by anaerobic bacteria to short-chain fatty acids, hydrogen, methane, and carbon dioxide in the large intestine. The production of butyrate from starch has received the most attention, because butyrate seems to possess several important functions in the large bowel, including antineoplastic properties. In 16.6% fecal homogenates, starch polysaccharides, whether digestible or resistant to in vitro hydrolysis by amylase, pectin, and glucose, were all completely degraded to equal amounts of short-chain fatty acids (mean 60 wt/wt%; range 49-67 wt/wt%). However, starch that was resistant to hydrolysis by amylase was much more slowly fermented with the production of proportionally less butyrate and propionate than digestible starch (butyrate, 15 and 33%, respectively; propionate, 3 and 20%, respectively). The daily intake of 35 g resistant starch (100 g amylomaize starch) by 7 ileostomy subjects increased ileal dry-matter effluent by 38 +/- 2 g/day, due exclusively to increased excretion of carbohydrates of nonfiber origin (starch-polysaccharides and oligo- and monosaccharides) from 14 +/- 1 to 51 +/- 2 g/day, with no change in excreted nonstarch polysaccharides, nitrogen, and ileal volume. The ileal excreted resistant starch increased the formation of total short-chain fatty acids by 50% in fecal homogenates incubated with ileal dry matter from the amylomaize starch period, with comparatively little effect on the ratio of produced butyrate. In fecal incubations, a considerable production of short-chain fatty acids (30-50%) was shown to be of noncarbohydrate (starch and nonstarch) origin, probably caused by the colonic degradation of ileal excreted peptides resistant to small-bowel absorption, because two thirds of the ileal excreted nitrogen was a-amino nitrogen (amino acids and peptides). In conclusion, the rate of short-chain fatty acid production from colonic fermentation of starch decreases as starch resistance to small-intestinal amylase degradation increases. Moreover, the percentage of butyrate produced is lower from resistant starch than from digestible starch. It is anticipated that ingestion of very resistant starch may result in its fecal excretion, when the time needed for its degradation exceeds colonic transit. Fiber, resistant starch, and now what can be called resistant protein are all precursors of colonic short-chain fatty acids, and any of them may become the main source as a result of dietary manipulation.