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 s mall intestine and is degraded by anaerobic bacteria to short-chain fa tty acids, hydrogen, methane, and carbon dioxide in the large intestin e. The production of butyrate from starch has received the most attent ion, because butyrate seems to possess several important functions in the large bowel, including antineoplastic properties. In 16.6% fecal h omogenates, starch polysaccharides, whether digestible or resistant to in vitro hydrolysis by amylase, pectin, and glucose, were all complet ely degraded to equal amounts of short-chain fatty acids (mean 60 wt/w t%; range 49-67 wt/wt%). However, starch that was resistant to hydroly sis by amylase was much more slowly fermented with the production of p roportionally less butyrate and propionate than digestible starch (but yrate, 15 and 33%, respectively; propionate, 3 and 20%, respectively). The daily intake of 35 g resistant starch (100 g amylomaize starch) b y 7 ileostomy subjects increased ileal dry-matter effluent by 38 +/- 2 g/day, due exclusively to increased excretion of carbohydrates of non fiber origin (starch-polysaccharides and oligo- and monosaccharides) f rom 14 +/- 1 to 51 +/- 2 g/day, with no change in excreted nonstarch p olysaccharides, nitrogen, and ileal volume. The ileal excreted resista nt starch increased the formation of total short-chain fatty acids by 50% in fecal homogenates incubated with ileal dry matter from the amyl omaize 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 degradati on of ileal excreted peptides resistant to small-bowel absorption, bec ause two thirds of the ileal excreted nitrogen was a-amino nitrogen (a mino acids and peptides). In conclusion, the rate of short-chain fatty acid production from colonic fermentation of starch decreases as star ch resistance to small-intestinal amylase degradation increases. Moreo ver, the percentage of butyrate produced is lower from resistant starc h than from digestible starch. It is anticipated that ingestion of ver y resistant starch may result in its fecal excretion, when the time ne eded for its degradation exceeds colonic transit. Fiber, resistant sta rch, and now what can be called resistant protein are all precursors o f colonic short-chain fatty acids, and any of them may become the main source as a result of dietary manipulation.