No abstract

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.

Medical Research Society 33P UDCA + CDCA (both of which decrease the molar ratio of cholesterol in bile) increased from 41% before, to 50% and to 72% after 5 and 10 mg of UDCA day-1 kg-' body weight respectively. There were concomitant decreases in the propor tions of both cholic acid and its bacterial metabolite, deoxycholic acid but the proportion of lithocholate increased from 4-5% before to 9·0% during therapy. There were no changes in liver function or fasting serum lipids during treatment and no patient developed diarrhoea.These results (i) show that treatment of non-obese gallstone patients with only 5 mg of UDCA day -1 kg -1 body weight consistently produces unsaturated bile and, (ii) confirm that, in the short term, UDCA causes neither diarrhoea nor hypertransaminaseaemia. UDCA continues to offer a promising alternative to CDCA for the medical treatment of gallstones.