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~_ _ _ _An in vitro faecal incubation system was used to study the metabolism of complex carbohydrates by intestinal bacteria. Homogenates of human faeces were incubated anaerobically with added lactulose, pectin, the hemicellulose arabinogalactan, and cellulose, both before and after subjects had been pre-fed each carbohydrate. Fermentation of added substrate was assessed by the production of short-chain fatty acids (SCFA) and suppression of net ammonia generation over 48 h of incubation. Control faecal homogenates to which carbohydrate was not added yielded an average increment of SCFA of 43 mmol/l, equivalent to 172 mmol/kg in the original stool. The addition of lactulose, pectin and arabinogalactan each increased the yield of SCFA by a similar amount, averaging 6.5 mmol/g carbohydrate or 1.05 mol/mol hexose equivalent; organic acid yield was not increased by pre-feeding these substances for up to 2 weeks. Acetate was the major SCFA in all samples at all times and, after pre-feeding with extra carbohydrate, butyrate concentrations exceeded propionate in all samples. Faecal homogenates incubated with cellulose showed no greater SCFA production than controls over the first 48 h, but there was a slight increase when samples from two subjects pre-fed cellulose were incubated for 14 d. Net ammonia generation was markedly suppressed by addition of lactulose to faecal incubates with an initial period of net bacterial uptake of ammonia. Pectin and arabinogalactan also decreased ammonia generation, but the reductions were not significant unless subjects were pre-fed these materials ; cellulose had no effect on ammonia generation.

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1. Sodium tartrate labelled with 14 C was given orally and parenterally to man and rats, and by direct injection into the caecum in rats. From the differences in urinary excretion after oral and parenteral administration intestinal absorption of tartrate was calculated as 18% of the dose in man and 81% in rats. Urinary tartrate was equivalent to 14% of the dose in man and 70% in rats, the differ ence between absorption and urinary excretion representing metabolism in body tissues.2. Both man and the rat excreted part of the U C as respiratory carbon dioxide. This occurred to a small extent after parenteral injection, suggesting metabolism of tartrate by body tissues, but was greater after oral or intracaecal administration, indicating that the main site of tartrate metabolism is the intestine.3. Several genera of intestinal bacteria were shown to liberate ["Clcarbon dioxide from labelled tartrate, and in a faecal incubation system Ltartrate, the natural isomer, was metabolized five times as rapidly as D-tartrate.4. Oral sodium L-tartrate, 1-5 mmol day -1 kg -1 , was given to two subjects and was shown to alkalinize the urine like sodium salts of other organic acids which are metabolized in the body. The reduction in renal hydrogen ion excretion showed that an average of 84% of the dose was metabolized.5. Only 5% of labelled tartrate given by mouth appeared in faeces, and pharmacological doses of unlabelled L-tartrate had little or no aperient effect.