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Besides being incorporated into proteins, Trp, an indispensable AA, is involved in numerous metabolic pathways. Previous data showed that Trp conversion into kynurenine (Kyn) and nicotinamide (Nam) differs among studies, and such differences cannot be explained by different dietary niacin supplies. We hypothesized that pig genotype influences Trp metabolism and thus the conversion of Trp into its metabolites. The objective of this study was to compare plasma appearance of Trp and related metabolites in 12 Duroc and 12 Piétrain crossbred postweaning pigs fed 2 contrasting dietary Trp levels. Within each genotype, 6 pigs were fed a basal (B-Trp: 17% and 15% standardized ileal digestible [SID] Trp:Lys for starter and prestarter diets) or supplemented (S-Trp: 24% and 23% SID Trp:Lys for starter and prestarter diets) Trp diet. Growth was monitored, and plasma fasted concentrations were measured over 4 wk, and then pigs were fitted with a jugular catheter for frequent blood samplings. After overnight fasting, 350 g of the experimental diets were offered to each pig, and plasma concentrations of Trp, Kyn, Nam, and 5-hydroxytryptamine (5-HT) were measured for 6 h. The activities of Trp-degrading enzymes were measured in different tissues collected after pig slaughtering. Plasma Trp fasted concentrations did not differ between B-Trp and S-Trp diets and increased from weaning to 2 and 4 wk after weaning for Piétrain but not for Duroc crossbred pigs (time × genotype, = 0.001). Plasma Kyn concentrations were greater 4 wk after weaning ( = 0.002) than at weaning and for Piétrain compared to Duroc genetics ( = 0.008). Plasma Nam concentrations were greater for pigs fed the S-Trp diet than for those fed the B-Trp diet ( = 0.0001) and for Duroc than for Piétrain genetic lines ( = 0.001); this difference tends to be greater at weaning than after ( = 0.055). Our data showed an increase in plasma concentrations of Trp, Kyn, Nam, and 5-HT according to time after a meal and to the dietary Trp content. However, postprandial plasma concentrations of Trp metabolites and enzyme activities were not significantly different between Duroc and Piétrain crossbred pigs. In conclusion, our results suggest that Nam endogenous synthesis capacity from Trp is greater in Duroc than in Piétrain crossbred pigs, but this was apparent only at weaning.

The present experiment aimed to determine if Trp metabolism and growth responses to dietary Trp are modulated by dietary niacin (B) in weanling piglets. Piglets weaned at 3 wk of age were distributed 1 wk later (7.6 kg of BW, SEM = 0.1) in 52 pens of 2 animals each. Pens were assigned to factorial dietary treatments with 2 additions of B, 15 mg/kg (LB3) vs. 45 mg/kg (HB3) and 2 additions of Trp, 0 mg/kg (-Trp) vs. 1 mg/kg (+Trp) for Trp to Lys ratios of 0.16 vs. 0.24, respectively. Growth performance was recorded every week from 4 to 10 wk of age. Fasting blood samples were taken at 4, 6, 8, and 10 wk of age. From 4 to 10 wk of age, ADFI tended to be greater ( = 0.10) in HB3 than in LB3 (1,031 vs. 1,003 g, SEM = 7), and this was reflected ( = 0.06) by ADG (642 vs. 623 g, SEM = 7). No treatment effect was observed on plasma Trp or kynurenine (Kyn), an intermediate metabolite of Trp catabolism. The response of plasma nicotinamide (Nam), a product of Trp catabolism and an indicator of B status, to dietary B differed according to treatments (interaction Trp × B, < 0.01) with values of 1.4, 3.3, 4.1, and 5.3 μM (SEM = 0.1) in LB3-Trp, HB3-Trp, LB3+Trp, and HB3+Trp, respectively. At 11 wk of age, postprandial blood samples were collected from 6 piglets per treatment for measurements of Trp and insulin metabolism. Postprandial plasma Trp (96.4 vs. 72.2 μ, SEM = 3.4) and Kyn (1.7 vs. 1.3 μ, SEM = 0.1) were greater ( < 0.01) in +Trp vs. -Trp. Postprandial plasma Nam was greater ( < 0.01) in +Trp vs. -Trp (3.4 vs. 1.9 µ, SEM = 0.3) and in HB3 vs. LB3 piglets (3.4 vs. 1.9 µ, SEM = 0.3). Postprandial peaks and areas under curves of C-peptide and glucose were not affected by treatments. However, for insulin, the postprandial peak was lower in +Trp vs. -Trp piglets in the LB3 group (interaction Trp × B, < 0.05); values were 1.3, 1.0, 0.7, and 1.0 n (SEM = 0.1) in LB3-Trp, HB3-Trp, LB3+Trp, and HB3+Trp, respectively. The peak value of the molar ratio insulin:C-peptide was lower ( < 0.02) in +Trp vs. -Trp piglets (0.56 vs. 0.73, SEM = 0.05). The responses observed on growth performance and plasma Nam suggest that the LB3 level was suboptimal. According also to plasma Nam, it appears that supplemental dietary B can attenuate Trp oxidation toward niacin metabolites. Postprandial profiles of insulin and C-peptide indicate that Trp action is exerted on insulin clearance rather than on insulin secretion in piglets, without apparent consequences on glucose utilization.

The objective of the study was to estimate Leu requirement for weaned piglets to balance indispensable AA in reduced CP diets. A dose-response experiment was conducted to estimate the standardized ileal digestible (SID) Leu to Lys ratio required for the maximum growth of young pigs after weaning. In this study, 96 female pigs (initial BW of 8 kg) were allotted to 1 of 6 dietary treatments with 16 individually penned pigs per treatment. Graded levels of crystalline L-Leu were added to a basal diet to provide diets containing 0.70, 0.80, 0.90, 1.00, 1.10, and 1.20 SID Leu:Lys. Lysine was limiting and fulfilled 90% of the current recommendations. The ADFI, ADG, and G:F were determined during a 2 wk experimental period. Blood and urine samples were taken at the end of each wk. The ADFI increased linearly (P < 0.001) from 0.70 to 0.80 SID Leu:Lys and then remained constant from 0.90 to 1.20 SID Leu:Lys. The ADG showed a quadratic increase ( P= 0.02), as the SID Leu:Lys level increased from 0.70 to 0.90 SID Leu:Lys and did not change further from 0.90 to 1.20 SID Leu:Lys. The G:F increased quadratically (P < 0.001) with increasing SID Leu:Lys level, and the greatest G:F was achieved with pigs receiving the diet with 0.80 SID Leu:Lys. Increasing the dietary SID Leu:Lys resulted in a linear increase in plasma Leu concentration (P < 0.001) and quadratic increases (P < 0.001) in plasma Cys concentration. The plasma concentration of most of the other AA was lowest in pigs receiving the diets with 0.90 to 1.00 SID Leu:Lys. The plasma urea nitrogen concentration tended (P = 0.08) to be lowest in pigs receiving 1.00 SID Leu:Lys, suggesting a more balanced AA profile at this level. Using a curvilinear-plateau model, the SID Leu:Lys requirement was estimated at 0.93 to maximize growth in female pigs weighing 8 to 12 kg.

Reducing the dietary CP level with free AA supplementation allows reduction of N excretion and the risk of gut disorders while maintaining performance of pigs. We have recently reevaluated the Val, Ile, His, and Leu requirements in pigs, which enables formulating very low CP diets. However, requirements for undifferentiated N, and thus the extent to which the dietary CP content can be reduced, are unknown. Two experiments were conducted to test the effect of reducing the dietary CP content to meet an ideal AA profile on N retention and performance in 10- to 20-kg pigs. In the first experiment, we measured N retention in 6 blocks of 4 pigs each, all receiving diets with 1.15% standardized ileal digestible (SID) Lys. Each pig within a block was allotted to different levels of dietary CP (19.7%, 16.8%, 14.0%, and 12.7%). The reduction of CP content from 19.7% to 16.8% had no impact on N retention and decreased N excretion by 29%. A further decrease in CP content to 14.0% and 12.7% resulted in a reduced N retention (P < 0.01). In the second experiment, we measured performance in 14 groups of 6 pigs each, allotted to 6 levels of dietary CP with 1.00% SID Lys with soybean meal (17.6%, 15.6%, 13.5%, and 11.8%) or without soybean meal (14.0% and 13.0%). Decreasing the dietary CP content from 17.6% to 13.5% had no effect on performance. Daily gain was reduced in pigs receiving the 11.8% CP diet (P < 0.01). Feeding the diet formulated without soybean meal with 13.0% CP content resulted in reduced feed efficiency, but the addition of Glu to increase the CP content from 13.0% to 14.0% restored performance (P < 0.01). In conclusion, the use of L-Val, L-Leu, L-Ile, L-His, and L-Phe enables a 4% unit reduction in the CP content relative to SID Lys in diets for pigs. Soybean meal can be totally replaced using cereals and free AA. However, a further reduction in dietary CP:Lys level below 13.5% reduces feed efficiency, indicating that the supply of N for the synthesis of dispensable AA may be a limiting factor for the performance of pigs.

The aim of the present study was to determine the minimum requirement of Ile in young pigs, enabling feeding of balanced low-CP diets. Most previous studies have used experimental diets that included blood cells, which are particularly high in Leu and known to antagonize the use of Ile. One week after weaning at d 28, 100 crossbred female pigs weighing 7.9 ± 0.7 kg were allocated to 1 of 5 dietary treatments. Diets were formulated to contain 1.15 g standardized ileal digestible (SID) Lys/MJ NE and were free of blood cells. The SID Ile was 0.42, 0.47, 0.53, 0.58, and 0.62 relative to Lys. The other indispensable AA were supplied according to requirements. Representative samples from the 5 diets were analyzed in 4 replicates at 3 different laboratories. The pigs were fed ad libitum and individually housed in 7 identical rooms during a 21-d period. At d 0, 7, 14, and 21, the pigs were weighed, and feed intake was determined. At d 15, blood samples were collected from the jugular vein to determine the plasma urea and free AA content. There were differences among the 3 laboratories in the analyzed content of several AA, and also Ile and Lys showed a large variation within the diets, which may cause variation in published requirement estimates. The concentration of Ile in plasma increased linearly (P < 0.01), and Lys in plasma decreased linearly (P = 0.02) with increasing SID Ile:Lys. A tendency for a linear decrease in plasma concentration was found for Thr (P = 0.10). Both ADFI and ADG were reduced when Ile was supplied above the Ile requirement estimate. Quadratic regression curves on ADFI, ADG, and G:F all showed the maximum at 0.52 SID Ile:Lys. Modeling with 2-sloped quadratic broken-line curves showed the maximum at 0.50, 0.53, and 0.54 SID Ile:Lys for ADFI, ADG, and G:F, respectively. In conclusion, the average estimation of requirement in this dose-response study using blood cell-free diets was 0.52 SID Ile:Lys during a 21-d experimental period from 8 kg BW.

When a diet deficient in Val with excessive Leu is offered to pigs, feed intake is reduced. The physiological mechanisms underlying the rejection of branched-chain AA (BCAA) unbalance are unknown. A meal pattern analysis was performed to determine how pigs respond to the ingestion of a diet unbalanced in BCAA to identify the mechanisms responsible for the aversive response of such a diet. Eight female pigs (initial BW of 30.7±1.7 kg at 9 wk of age) received alternatively a diet either unbalanced in BCAA supply (i.e., a diet deficient in Val with an excess supply of Leu) or a control diet (i.e., a diet with a sufficient supply of Val with an excess supply of Leu) during 4 periods of 5 consecutive days. Feed consumption was monitored continuously to determine feeding behavior. Average daily feed intake of pigs receiving the diet unbalanced in BCAA was l3% less than that in pigs offered the control diet (P<0.01). Offering the unbalanced diet had no effect on meal size but reduced the number of meals from 9.9 to 8.5 per day (P<0.01). There was no difference between diets in intermeal interval but a slight trend for an increased meal duration from 14.5 to 16.3 min in pigs receiving the unbalanced diet (P=0.13). The rejection of feed appeared within the first 2 d after offering the unbalanced diet. The results of this experiment indicate that the BCAA unbalanced diet had no effect on satiety and satiation. After initiation of a meal, pigs ate a normal-sized meal and were hungry, but the increase in meal duration and a decrease in the number of meals inferred a negative alliesthesia (less pleasant) response to the BCAA unbalanced diet. On the basis of meal patterns, the rejection of a diet unbalanced in BCAA may not involve short-term mechanisms related to oropharyngeal and gastrointestinal receptors but may be triggered by postabsorptive signals.

Indispensable AA are involved in the control of feed intake. When a diet deficient in Val is offered to pigs, feed intake is typically reduced. This effect is aggravated when dietary Leu is supplied in excess of the requirement. If an unbalanced supply of branched-chain AA (BCAA) is harmful, an anorectic response may serve as a mechanism to prevent this situation. We verified this hypothesis by measuring the voluntary feed intake of a balanced diet offered during the 30-min period 1 h after ingestion of a test meal deficient or not in Val (Val- and Val+) with an excess of Leu. Twelve and four 6-wk-old crossbred female pigs were used in Exp. 1 and 2, respectively. Prior ingestion of the Val- test meal resulted in a 14% reduction in feed intake compared with that observed after ingestion of the Val+ test meal (P = 0.06) in Exp. 1, indicating that the signal to reduce feed intake occurred within 1 h. It is possible that the plasma concentration of the limiting AA serves as a signal for the dietary AA deficiency. We therefore determined the postprandial plasma concentrations of BCAA and their α-keto acids after ingestion of Val- and Val+ in 4 pigs in Exp. 2. After ingestion of the Val- diet, plasma concentrations of Val and its keto acid were reduced compared with values observed after ingestion of the Val+ diet. The peak concentration occurred earlier after ingestion of the Val- diet compared with that of the Val+ diet. Although the plasma concentration increased after the meal, it declined rapidly in pigs offered Val-, and the Val concentration 4 h after ingestion of the meal was even less than that observed in the fasted state. In conclusion, it appears that the pig is able to detect a deficient supply of Val within 1 h after ingestion. The plasma concentration of Val or its concentration relative to the other BCAA during the postprandial period may act as a signal indicating the AA deficiency.