Dietary Tryptophan Concentration Research Articles

Dietary tryptophan requirement of hybrid striped bass (Morone chrysops x M. saxatilis)

Requirements for six of the 10 indispensable amino acids (IAA) have not been quantified for hybrid striped bass. In this study, we estimate the requirement for l-tryptophan by nonlinear regression analysis of several growth indicators. Fifteen isocaloric, isonitrogenous diets were formulated to contain 1.0, 1.3, 1.6, 1.9, 2.2, 2.5, 2.8, 3.1, 3.4, 3.7, 4.0, 5.0, 6.0, 10.0 or 14 g L-tryptophan kg-1 diet and fed to reciprocal cross hybrid striped bass for 7 weeks. After 5 weeks, survival of fish receiving the basal diet was 40% while surviving fish fed this diet were in poor health. Survival of fish receiving 1.3 g Trp kg-1 diet declined to 70% by termination of the trial. Survival in other treatments was 100%. Fish weight gain was 100% or greater for fish receiving 1.6 g Trp kg-1 diet or more. Hepatosomatic index, muscle ratio and intraperitoneal fat (IPF) ratio also responded to dietary tryptophan concentration. IPF was inversely related to dietary tryptophan concentration. The dietary tryptophan requirement was estimated to be between 2.1 and 2.5 g kg-1 diet (6-7 g kg-1 protein), depending on response variable, using four- and five-parameter saturation kinetics models. These findings will increase the precision of diets formulated for hybrid striped bass.

Dietary tryptophan requirement of fingerling Indian major carp, Cirrhinus mrigala (Hamilton)

An 8-week feeding trial was conducted to evaluate the effects of dietary tryptophan concentration on weight gain and feed efficiencies of fingerling Indian major carp, Cirrhinus mrigala. Six isonitrogenous (40% crude protein) and isocaloric (17.90 kJ g−1) amino acid test diets containing casein, gelatin and l-crystalline amino acids with graded levels of l-tryptophan (0.06, 0.16, 0.26, 0.36, 0.46 and 0.56 g 100 g−1 dry diet) were formulated. Fish (4.25±0.30 cm, 0.62±0.02 g) were randomly stocked in triplicate groups in 70 L (water volume 55 L) flow-through (1–1.5 L min−1) indoor circular tanks and fed experimental diets at 5% of their body weight/day in two feedings at 08:00 and 16:00 hours. Maximum live weight gain (277%), lowest feed conversion ratio (FCR) (1.50) and highest protein efficiency ratio (PER) (1.66) were measured at 0.36% dietary tryptophan. The relationship between dietary tryptophan levels and weight gain, FCR and PER data were described using second-degree polynomial regression analysis indicating the tryptophan requirement at 0.42, 0.39 and 0.38 g 100 g−1 of dry diet respectively. Whole body moisture decreased with increasing tryptophan up to 0.36%. Significantly (P<0.05) higher protein content was evident in fish fed diet containing 0.36% tryptophan. Body fat increased significantly (P<0.05) in fish fed with different tryptophan concentrations except those fed 0.36% tryptophan where a significantly lower fat content was noted. Significantly (P<0.05) higher ash content was reported at 0.06% and 0.16% tryptophan levels. Survival was 100% in fish fed all the diets except those fed 0.06% tryptophan. Based on the results, diets for fingerling C. mrigala should contain tryptophan at 0.38 g 100 g−1 dry diet, corresponding to 0.95 g 100 g−1 dietary protein for optimum growth and efficient feed utilization.

Requirement of tryptophan in relation to the supply of large neutral amino acids in laying hens

The present study was undertaken to find out whether the tryptophan requirement of laying hens is influenced by the supply of large neutral amino acids (LNAA). A factorial experiment was performed in which the dietary tryptophan concentration was varied at six different levels (1.0, 1.25, 1.5, 1.75, 2.0, and 2.5 g tryptophan/kg diet). As the second factor, the dietary concentrations of LNAA (isoleucine, valine, leucine, phenylalanine, and tyrosine) were varied at two levels. The first level provided an adequate supply of these amino acids; at the second level the concentrations of these amino acids were 40% higher than at the first level. The tryptophan requirement was estimated by a broken-line model and an exponential model of regression analysis. The tryptophan intake required for optimum (100% of maximum in the broken-line model, 95% of the maximum in the exponential model) egg production and daily egg mass was lower in hens fed the diets with high LNAA concentrations (145 and 155 mg/hen per day, respectively, in average of both models) than in hens fed the diets with adequate concentrations of LNAA (184 and 198 mg/hen per day, respectively, in average of both models). In contrast, the tryptophan requirement for optimum BW gain was lower in hens fed the diets with adequate LNAA concentrations (178 mg tryptophan per day) than in hens fed the diets with a high concentration of LNAA (212 mg tryptophan per day). In conclusion, the study suggests that an interaction between dietary LNAA and tryptophan exists in laying hens.

Interactions of various supplies of isoleucine, valine, leucine and tryptophan on the performance of laying hens

The present study was undertaken to investigate the interactions among the supplies of isoleucine, leucine, valine, and tryptophan in laying hens. A three-factor trial was conducted with laying hens in which the dietary concentrations of isoleucine (5.7, 8.0, and 11.5 g/kg), valine and leucine (6.3 and 7.2 g/kg and 10.1 and 11.5 g/kg, respectively), and tryptophan (1.5 and 2.4 g/kg) were varied. At the lowest concentration of valine + leucine, an increase in dietary isoleucine concentration led to a dose-dependent reduction in feed consumption, daily egg mass, and body weight gain and an increase of the isoleucine concentration in plasma. At a high dietary concentration of valine + leucine, excess dietary isoleucine concentration caused only a weak depression of performance parameters; the isoleucine concentration in plasma was independent of the dietary isoleucine concentration. Increasing the dietary tryptophan concentration did not influence the effect of an excessive dietary isoleucine concentration on performance parameters. Increasing the tryptophan concentration from 1.5 to 2.4 g/kg diet did, however, lead to a significant increase in feed consumption, irrespective of the supply of isoleucine, valine, and leucine. In conclusion, our study demonstrates that the supply of valine + leucine influenced the effects of excess dietary isoleucine in laying hens, whereas the supply with tryptophan did not.

Studies on the tryptophan requirement of piglets

Three experiments were conducted to determine the requirement of tryptophan for piglets. In the first two experiments dose‐response relationships between the dietary tryptophan concentration and performance criteria of piglets were examined in order to determine the dietary tryptophan concentration required for maximum performance. In the first experiment dietary tryptophan levels ranged from 1.09 to 2.32 g per kg, in the second experiment they ranged from 1.70 to 2.60 g per kg. In both experiments a close correlation was observed between the dietary tryptophan concentration and piglet performance criteria (feed intake, daily gains, feed efficiency). In the first experiment, regression analysis using a non‐linear model revealed that the optima, defined as 95% of the asymptotic response in the model used, for feed intake and daily gains were achieved at tryptophan levels in excess of the highest concentration of 2.32 g per kg feed. The performance level of the piglets in this experiment was generally very low, however. In the second experiment feed intake, the optimum tryptophan concentration, defined as 95% of the asymptotic response, for daily gains and feed efficiency were achieved within a small range between 2.07 and 2.14 g tryptophan per kg feed, corresponding to 1.84 to 1.91 g precaecal digestible tryptophan per kg feed or 0.153 to 0.159 g tryptophan per MJ ME. These results suggest that the tryptophan concentration for maximum performance of piglets is probably higher than has been implied in numerous studies to date. The third experiment was set up to investigate the effect of the reduced feed intake and the effect of an inadequate tryptophan supply per se on the animals’ growth. Here a two‐factorial experimental design was used also by varying the energy density of the diet (13 vs. 14MJ ME per kg feed). In addition to tryptophan deficient groups (1.5 g tryptophan per kg feed), this experiment contained conventional control groups (2.6 g tryptophan per kg feed, ad libitum feeding) and pair‐fed control groups (2.6 g tryptophan per kg feed, feed intake identical to that of the tryptophan deficient group). The energy density had no significant effect on the animals’ performance and increasing the energy density of the diet did not significantly affect feed and energy intake or daily gains of the tryptophan deficient animals. Feed intake, daily gains and feed efficiency of the fryptophan deficient groups were markedly poorer (by 30, 35 and 10%) than in the ad libitum control groups. When compared with the pair‐fed control groups, on the other hand, the performance of the tryptophan deficient groups in terms of daily gains, feed conversion and energy efficiency was only slightly and not significant lower by 1, 4 and 3%, respectively. These results demonstrate conclusively that the growth depression in tryptophan deficiency is almost entirely due to the marked reduction in feed intake rather than to a direct limitation of protein accretion caused by an inadequate tryptophan supply.

Incidence of pecking damage in growing bantams in relation to food form, group size, stocking density, dietary tryptophan concentration and dietary protein source

1. This paper reports 4 experiments with groups of 10 to 20 growing bantams in multi-unit brooders, which investigated effects of certain environmental and dietary factors on development of feather pecking damage to 6 weeks of age. Damage was assessed according to a subjective scoring system. 2. A test of food form (pellets, mash, mash diluted with 100 g/kg powdered cellulose) confirmed that pecking damage tends to be greater with pellets than with mash but there was no significant difference between the low damage scores associated with undiluted and diluted mash treatments. 3. A test of group size (10, 20 birds) and stocking density (744, 372, 186 cm2/bird) showed that variation in pecking damage was associated with group size density interactions. 4. A test of dietary supplementation with L-tryptophan (0, 10, 20 g/kg) showed suppression of pecking damage with the higher (20 g/kg) dose, compared with the control (0 g/kg) treatment. 5. A test of dietary protein source (plant, mainly animal, mainly semipurified) showed no difference in pecking damage scores between treatments.

Feather pecking damage in growing bantams is influenced by dietary tryptophan concentration but not dietary protein source

Feather pecking damage in growing bantams is influenced by dietary tryptophan concentration but not dietary protein source

Tryptophan Reduces Hepatic Lipid Accumulation Induced Experimentally by Refeeding after Starvation or Estrogen Administration in Broiler Chicks.

Two experiments were conducted to study the effects of dietary L-tryptophan supplementation on hepatic lipid accumulation in broiler chicks. Male broiler chicks were treated with 3 days refeeding after starvation or administrations of dienestrol diacetate (0.01% in diet) for 12 days. Low tryptophan diet (0.12%) was formulated and supplemented to provide the specified concentrations of tryptophan (0.12-0.46%). Supplementation of L-tryptophan beyond the requirement for growth reduced the liver weight and liver lipid content expressed as per unit feed intake in the starved-refed chicks. Either higher or lower dietary tryptophan concentration compared with the requirement decreased the liver weight and liver lipid content in the estrogen-administered chicks. These results demonstrate tryptophan supplementation beyond the requirement reduces the hepatic lipid accumulation induced experimentally in broiler chicks.

Tryptophan requirement of growing swine as determined by the oxidation of an indicator amino acid.

The tryptophan requirement of growing swine was determined using the oxidation of L-[1-14C]-phenylalanine as an indicator of the adequacy of the dietary tryptophan level. Forty crossbred boars (30 to 45 kg) were fed a basal diet containing 16% protein supplied by corn and gelatin. A series of experimental diets containing .05, .08, .10, .15, .20 and .25% L-tryptophan were prepared. The diets were supplemented with crystalline amino acids to provide 135% of the recommended levels. Release of 14CO2 was measured for 1 h following a meal of the experimental diet containing 20 microCi 14C phenylalanine. Increasing dietary tryptophan from .05 to .13% decreased release of 14CO2. Further increases in dietary tryptophan concentration did not significantly influence 14CO2 production. Regression analysis using a two-phase linear regression crossover model indicated that phenylalanine oxidation was minimized by a dietary tryptophan concentration of .13%. It was concluded that at a concentration of .13%, tryptophan was no longer limiting the retention of the other amino acids, thus this is the requirement for maximum protein retention by the young, growing boar.

The effects of dietary tryptophan levels on growth and metabolism of rainbow trout (Salmo gairdneri).

Groups of rainbow trout (Salmo gairdneri) (mean weight 14 g) were given diets containing 0.8, 1.3, 2, 3, 4 or 6 g tryptophan/kg diet for 12 weeks. By analysis of the growth results, the dietary requirement of tryptophan was found to be 2.5 g/kg diet (equivalent to 50 mg/kg biomass per d). Carbon dioxide expired by trout following intraperitoneal injection of [14COOH]tryptophan contained little radioactivity when dietary tryptophan level was low but, above 2.0 g/kg diet, it increased rapidly with increasing dietary tryptophan level. The break point in the dose-response curve did not, however, coincide with that from the growth results. Changes in concentrations of free tryptophan in blood and liver and activity of hepatic tryptophan pyrrolase (EC 1. 13. 11. 11) in response to changes in dietary tryptophan concentration did not provide reliable indicators for quantifying dietary requirement. Unlike the situation in mammals, blood tryptophan was not protein-bound to any appreciable extent. Tryptophan pyrrolase of trout has properties which suggest it has no apoenzyme form. In fish given adequate levels of tryptophan injected intraperitoneally with a tracer dose of [14COOH]tryptophan, 60% of the dose was incorporated into body protein within 1 d. The turnover of the label in this protein is very slow. Those trout given diets deficient in tryptophan suffered from severe scoliosis and lordosis as well as having increased liver and kidney levels of calcium, magnesium, sodium and potassium.

The tryptophan requirements of young laying pullets.

Two experiments were conducted with laying pullets between 32 and 47 weeks of age. In each trial 1728 White Leghorn and 1728 cross-bred pullets were used. A series of diets of increasing protein content was offered. Protein quality was identical in all diets and tryptophan was demonstrated to be the most limiting amino acid in the protein mixture used. The daily tryptophan requirement of the individual pullet was estimated, by indirect methods, to be 2.25 mg/g egg output plus 10.25 mg/kg body weight. Response curves for flocks of pullets are illustrated. Calculated optimum intakes of tryptophan for various ratios of costs of input to value of output are tabulated. It is estimated that for a flock of mean body weight 1.5 kg, producing 55 g egg mass/hen d and consuming 110 g food/hen d, the optimum dietary tryptophan concentration is 1.7 g/kg when the marginal cost of supplying 1 kg tryptophan is 20 times the marginal value of 1 kg egg output.

Urinary Excretion of Indoxyl Sulfate (Indican) by Human Subjects Ingesting a Semisynthetic Diet Containing Variable Quantities of l-Tryptophan

The excretion of indoxyl sulfate by four groups of disease-free human subjects ingesting a semisynthetic diet containing variable quantities of l-tryptophan was measured. As the tryptophan content of the diet was altered, the urinary excretion of indican varied directly. When tryptophan was administered to one of the groups at least 8 hours after the ingestion of the other amino acids, then indoxyl sulfate excretion was not augmented. Over a wide range of dietary tryptophan levels, a constant fraction of about 3 per cent appeared in the urine as indican. As the dietary tryptophan concentration became very low and approached zero, abundant quantities of indican continued to be excreted in the urine. These data suggested that tryptophan derived from gastrointestinal secretions, shed mucosal cells, intestinal bacteria or transported from the serosal to the mucosal side of the intestine provided a significant source of indican.