PATHWAYS OF ACETATE, PROPIONATE, AND BUTYRATE FORMATION BY THE HUMAN FECAL MICROBIAL-FLORA

The pathways of short-chain fatty acid (SCFA; acetate, propionate, and butyrate) formation from glucose were determined for the human fecal microbial communities of two subjects, The pathways were identified by radioisotope analysis of the SCFA and CO2 obtained after incubation o f fecal suspensions with glucose under 20% CO2 with [1-C-14]glucose, [ 3,4-C-14]glucose, or (CO2)-C-14. Acetate was chemically degraded to le arn the labeling of the methyl and carboxyl carbons. The labeling of C O2 and acetate showed that the major route of glucose catabolism was t he Embden-Meyerhof-Parnas pathway, with production of CO2 from pyruvat e carboxyl carbon. Labeling of the methyl and carboxyl carbons of acet ate by (CO2)-C-14 or [3,4-C-14]glucose proved that acetate was formed from CO2 by the Wood-Ljungdahl pathway, CO2 reduction accounted for ab out one-third of the acetate formed by suspensions from subject 1 and about one-fourth of the acetate formed by suspensions from subject 2. Propionate was formed by a CO2 fixation pathway, and butyrate was form ed by classical routes of acetyl-S coenzyme A condensation. The amount of CO2 formed from [1-C-14] glucose and acetate labeling patterns obt ained with the other C-14 precursors indicated that the Entner-Doudoro ff, transketolase-transaldolase, and heterolactic pathways were not si gnificant. Fermentation of cabbage cellulose by subject 1 followed the same pathways as were used for glucose. The results with suspensions from subject 2 suggested that some radioactive acetate was formed from the C-3 of glucose by the Bifidobacterium pathway.