Acetate production from hydrogen and [13C]carbon dioxide by the microflora of human feces

Abstract

Fecal suspensions from humans were incubated with 13Co2 and H2. The suspensions were from subjects who harbored 108 and 1010 methanogens per g (dry weight) of feces, respectively, and from a subject who did not harbor methanogens. Quantitative nuclear magnetic resonance spectroscopy showed that acetate labeled in both the methyl and carboxyl groups was formed by suspensions from the subject without methanogens and the subject with the lower concentrations of methanogens. The amounts of labeled acetate formed were in agreement with the amounts expected based on measurements of H2 utilization. No labeled acetate was formed by suspensions from the subject with the higher concentrations of methanogens, and essentially all of the H2 used was accounted for by CH4 production. Suspensions from the subject with lower concentrations of methanogens produced both methane and acetate from H2 and CO2. The results indicate that reduction of CO2 to acetate may be a major pathway for microbial production of acetate in the human colon except when very high concentrations of methanogens (ca. 1010 per g [dry weight] of feces) are present. Double-labeled acetate was also formed from H2 and "3CO2 by fecal suspensions from nonmethanogenic and moderately methanogenic rats.

Microbial H2/CO2 acetogenesis in animal guts: nature and nutritional significance

“…Since acetate can be absorbed from the rodent cecum and oxidized for energy [8,9], these data taken together with those of Yang et al [8] on the contribution of cecal acetate to rat nutrition, suggest that H2/CO 2 acetogenesis in rat ceca could support up to 0.25% of the animal's maintenance energy requirement. Recently, Lajoie et al [10] confirmed the findings of Prins and Lankhorst by using rat fecal contents, but they also found that rats from their colony were moderately methanogenic. Fecal suspensions used about 1/2 the added H2 for methanogenesis, the rest was used for acetogenesis.…”

“…Methane (0.03-3 liters per day) is produced in the large intestine of 1/3 to 1/2 of all adult humans as a result of H2/CO 2 methanogenesis [19]. Wolin and Miller [19] hypothesized that in 'nonmethanogenic' individuals CO 2 reduction to acetate occurs, and recent experiments have shown that the magnitude of H2/CO z acetogenesis in fecal suspensions varies inversely with the number of viable methanogens (and methanogenie activity) in feces ( [10]; Table 2). Although a total synthesis of [t3C]acetate from t3co2+ Ha occurred with some fecal suspensions, it will still be important to verify that the process occurs during fermentation of normal colonic substrates (e.g.…”

“…Although a total synthesis of [t3C]acetate from t3co2+ Ha occurred with some fecal suspensions, it will still be important to verify that the process occurs during fermentation of normal colonic substrates (e.g. cellulose or bemicelluloses) and that interspeciesderived H a is the relevant reduetant in situ [10]." Nevertheless, one can estimate the potential impact of H:/CO2 acetogenesis on human nutrition as follows.…”

“…If the daily basal metabolic requirement for adults is about 7113 kJ [22], then ap- Comprehensive studies of H2/CO 2 acetogens in the human colon have not yet been done. However, Peptostreptococcus productus and Eubacterium limosum, known carbohydrate-fermenting species in the colon, can also use H e + CO 2 as growth substrates [10,19].…”

Metabolic interactions involving sulphate-reducing and methanogenic bacteria in the human large intestine

“…These data confirm that MB and SRB were involved in H 2 metabolism in each individual. Other possible mechanisms of H 2 disposal in the colon include diffusional losses in breath and flatus, or the existence of alternative bacteriological oxidative processes such as dissimilatory nitrate reduction [25] or acetogenesis [41]. Although energetically less favourable than SO 2reduction or methanogenesis [42], acetogenesis in the large bowel may be favoured by the low pH environment of the proximal colon.…”