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1. L-histidine (20 g/kg) added to vitamin B12-deficient and cyanocobalamin-supplemented diets based on soya-bean flour reduced the growth of rats given the vitamin B12-deficient diet but stimulated growth of rats given the cyanocobalamin-supplemented diet. Liver weight (g/kg body-weight)increased, but the protein content of the livers decreased, in rats given histidine supplements. The histidine was associated with significantly higher folate concentrations in the livers of cyanocobalamin-supplemented rats.

Rats fed on vitamin B12-deficient or vitamin B12-supplemented diets and treated with phenobarbitone by intraperitoneal injection for 5 d showed significant increases in the activity of glutamate formiminotransferase in liver. The only significant depletion in liver folate activity was in vitamin B12-supplemented rats that were starved for 48 h. When rats were given the same diets, with phenobarbitone and diphenylhydantoin added, for 12 weeks or more in two separate experiments, significant increases in transferase activity were found only in the livers of animals fed on the deficient diet. However, there was significant depletion of liver folate in animals taking the supplemented diet.

1. Kidney-cortex slices and the perfused livers of vitamin B(12)-deficient rats removed propionate from the incubation and perfusion media at 33 and 17% respectively of the rates found with tissues from rats receiving either a normal or a vitamin B(12)-supplemented diet. There was a corresponding fall in the rates of glucose synthesis from propionate in both tissues. 2. The addition of hydroxocobalamin or dimethylbenzimidazolylcobamide coenzyme to kidney-cortex slices from vitamin B(12)-deficient rats in vitro failed to restore the normal capacity for propionate metabolism. 3. Although the vitamin B(12)-deficient rat excretes measurable amounts of methylmalonate, no methylmalonate production could be detected (probably because of the low sensitivity of the method) when kidney-cortex slices or livers from deficient rats were incubated or perfused with propionate. 4. The addition of methylmalonate (5mm) to kidney-cortex slices from rats fed on a normal diet inhibited gluconeogenesis from propionate by 25%. 5. Methylmalonate formation is normally only a small fraction of the flux through methylmalonyl-CoA. This fraction increases in vitamin B(12)-deficient tissues (as shown by the urinary excretion of methylmalonate) presumably because the concentration of methylmalonyl-CoA rises as a result of low activity of methylmalonyl-CoA mutase (EC 5.4.99.2). Slow removal of methylmalonyl-CoA might depress propionate uptake owing to the reversibility of the steps leading to methylmalonyl-CoA formation.

The effect of ether and pentobarbitone anaesthesia on gastrointestinal motility and absorption has been studied by measuring simultaneously gastric emptying, small intestinal transit and intestinal absorption of glucose and iodide in intact rats. Both gastric emptying and intestinal transit are very slow under ether anaesthesia, but with pentobarbitone there is no significant delay. The absorption of glucose by the small intestine is significantly impaired by ether but not by pentobarbitone, and a tracer dose of iodide is absorbed normally under both forms of anaesthesia.