To study the absorption of microbial lysine in growing rabbits, a labelled diet (supplemented with 15NH4Cl) was administered to six animals (group ISOT); a control group (CTRL, four rabbits) received a similar, but unlabelled, diet. Diets were administered for 30d. An additional group of six animals were fed the unlabelled diet for 20d and then the labelled diet for 10d while wearing a neck collar to avoid caecotrophy (group COLL), in order to discriminate it from direct intestinal absorption. At day 30 animals were slaughtered and caecal bacteria and liver samples taken. The 15N enrichment in amino acids of caecal bacteria and liver were determined by GC–combustion/isotope ratio MS. Lysine showed a higher enrichment in caecal microflora (0·925 atom% excess, APE) than liver (0·215 APE) in group ISOT animals, confirming the double origin of body lysine: microbial and dietary. The COLL group showed a much lower enrichment in tissue lysine (0·007 (se 0·0029) APE for liver). Any enrichment in the latter animals was due to direct absorption of microbial lysine along the digestive tract, since recycling of microbial protein (caecotrophy) was avoided. In such conditions liver enrichment was low, indicating a small direct intestinal absorption. From the ratio of [15N]lysine enrichment between liver and bacteria the contribution of microbes to body lysine was estimated at 23%, with 97% of this arising through caecotrophy. Absorption of microbial lysine through caecotrophy was 119 (se 4·0) mg/d, compared with 406 (se 1·8) mg/d available from the diet. This study confirms the importance of caecotrophy in rabbit nutrition (15% of total protein intake).

This study investigates the effects of increased NH3 or amino acid supply on glutamine utilisation and production by the splanchnic tissues of fed sheep. Six sheep, prepared with vascular catheters in the aorta, mesenteric, portal and hepatic veins, were fed grass pellets to 1·1×energy maintenance requirements. Each treatment involved a 4 d abomasal infusion, of either ammonium bicarbonate (AMM; 23·4 μmol/kg0·75 per min), water (CONT), or a mixture of amino acids that excluded glutamine and glutamate (AA; 46·8 μmol amino acid-N/kg0·75 per min). The treatments simulated nutritional extremes in terms of the balance of absorbed N. Kinetics across the whole gut and the liver were monitored during an intra-jugular infusion of [5-15N]glutamine. Blood flow across the whole gut or liver were unaffected by treatment. Both AMM and AA infusions doubled the hepatic release of urea-N compared with CONT (P<0·02). AA infusion decreased arterial glutamine concentration by 26 % (P<0·01) and 23 % (P<0·05) compared with AMM and CONT respectively. Despite this, whole-body glutamine flux was not affected by treatment. In contrast, AMM infusion increased hepatic glutamine production by 40 % compared with CONT (P<0·02). This provided a mechanism to ensure NH3 supply to the periphery was maintained within the normal low physiological levels. Hepatic glutamine utilisation tended to increase during AA infusion, probably to ensure equal inflows of N to the ornithine cycle. Between 6 and 10 % of NH3 absorbed across the digestive tract was derived from the amido-N of glutamine. Overall, splanchnic glutamine utilisation accounted for 45–70 % of whole-body glutamine flux.