Seven non-anaesthetized pigs (mean body-weight 64.6 kg) were used to study the intestinal absorption and hepatic metabolism of glucose and amino acids (AA) using carbohydrate solutions (maltose dextrin; 440 g/2 l), containing 110 g of either an enzymic milk-protein hydrolysate (PEP) with a large percentage of small peptides (about 50% with less than five AA residues) and very few free AA (8%) or a mixture of free AA (AAL) with an identical pattern, infused intraduodenally. Each pig was previously fitted under anaesthesia with electromagnetic flow probes around the portal vein and the hepatic artery, and with permanent catheters in the portal vein, carotid artery, one hepatic vein and the duodenum. Each solution was infused for 1 h after a fasting period (18 h) and each pig received both solutions at 8 d intervals. The observation period lasted 8 h. For most AA (his, lys, phe, thr, arg, tyr, pro) the absorption rate after infusion of PEP was significantly higher than after that of AAL during the 1st hour, but the differences quickly disappeared. After 8 h, the only differences concerned his and tyr (PEP > AAL) and met, glu and asp (AAL > PEP). There was a large uptake of blood AA by gut-wall cells, higher after AAL infusion than after PEP infusion, particularly for branched-chain AA (BCAA). The absorption of ammonia-nitrogen after both infusions was equivalent to two-thirds of urea-N passing from blood to intestinal tissues and lumen. Glucose absorbed within 8 h represented only 76% (PEP) or 69% (AAL) of the infused amounts. The cumulative hepatic total AA (TAA) uptake increased from 13 to 27% of the infused amounts between the 1st and the 8th hour after PEP infusion, and from 8 to 31% after AAL infusion. Most essential AA were largely taken up by the liver, with the exception of met (PEP) and thr and of BCAA, which were poorly retained for both solutions; there was a high uptake of ala and gly, and a release of asp, glu, and gln. Urea-N released by the liver within 8 h was equivalent to 23–25% absorbed amino-N and to around 1.5 times ammonia-N taken up by the liver within 8 h. Glucose was highly taken up by the liver during the first hours then released, the total uptake within 8 h representing about half the absorbed amount. There was a lactate release tending to be higher after PEP than after AAL infusion and a liver pyruvate release identical for both solutions. From calculations of net non-catabolic metabolism in the liver the possible synthesis of liver proteins within 8 h may be estimated at 35 g for both solutions. The cumulative peripheral TAA uptake increased from 12 to 27% of the infused amounts between the 1st and 8th hour after PEP and from 9 to 11% after AAL infusion. At 8 h after the infusion the larger uptake concerned BCAA, arg, glu and asp and there was a marked release of gln, gly and ala for both solutions; the peripheral balance was zero for met (PEP) or characterized by a release of phe and thr (AAL). Thus, protein synthesis seemed only to be possible with the aid of plasma proteins synthesized in the liver. The 8 h peripheral balance of glucose, lactate and pyruvate was characterized by the same level of uptake for both solutions. The time-course of AA absorption, depending on the physicochemical structure of nitrogenous mixtures present in the digestive tract, had an influence on the pattern of liver and peripheral AA uptake.