Dietary Tryptophan Levels Research Articles

Effect of Dietary Tryptophan Levels on the Urinary Excretion of Nicotinamide and Its Metabolites in Rats Fed a Niacin-Free Diet or a Constant Total Protein Level

We previously found that the sum total urinary excretion of nicotinamide and its metabolites in growing rats did not increase as the level of dietary casein increased. So, we investigated how the urinary excretion of nicotinamide and its metabolites changed when rats were fed nicotinic acid-free diets containing 10, 20 or 40% casein, or when they were fed diets containing nicotinic acid and the same level of protein but different levels of tryptophan. The latter diets were 10% casein-30% gelatin, 20% casein-20% gelatin or 40% casein. With the nicotinic acid-free diets, the sum total urinary excretion of nicotinamide and its metabolites was almost the same in the groups fed the 20 and 40% casein diets; however, it was significantly lower in the group fed the 10% casein diet. With diets containing the same level of protein, the sum total urinary excretion of these compounds in the groups fed the 10% casein-30% gelatin, 20% casein-20% gelatin and 40% casein diets were about 5, 7 and 11 mumol/d, respectively, values that were significantly different from each other. Therefore, it was found that only when the total protein intake was constant did the sum total urinary excretion of nicotinamide and its metabolites increase with increasing intake of tryptophan.

The Influence of Dietary Tryptophan on Broiler Chick Growth and Lipid Metabolism as Mediated by Dietary Protein Levels

Three experiments were conducted to determine how dietary protein and tryptophan influence the lipid metabolism of growing broiler chicks. A diet-dilution method (corn-com gluten meal-gelatin summit/corn starch basal) was used in three factorial experiments. Various levels of protein and tryptophan were fed in each experiment: protein from 16 to 28% and tryptophan from .34 to 2.74% of protein.Gain was maximized when the dietary levels of tryptophan were .83 ± .03, .77 ± .04, .77 ± .05, and .78 ± .05% of the protein for 16, 20, 24, and 28% dietary protein, respectively. The requirement estimates for feed efficiency and gain were similar. Liver lipids significantly decreased as the level of dietary tryptophan increased at each protein level (P<.0001). Dietary tryptophan did not significantly alter the concentration of total plasma lipid in the chicks or in die carcass lipid content (P>.2399). Tryptophan supplementation significantly increased the concentration of plasma linoleic acid and plasma free tryptophan.The requirement of the chicks for tryptophan was estimated to be .80 ± .01% of the dietary protein for the growing chick. Increased liver lipid and decreased plasma tryptophan are diagnostic lesions suggesting a tryptophan deficiency.

Effect of dietary tryptophan on plasma and brain tryptophan, brain serotonin, and brain 5-hydroxyindoleacetic acid in rainbow trout

In order to determine the effect of dietary tryptophan level on plasma and brain tryptophan, brain serotonin, and brain 5-hydroxyindoleacetic acid levels, juvenile rainbow trout ( Salmo gairdneri) were raised for 16 weeks on semipurified diets containing 0.06%, 0.16%, 0.21%, 0.26%, 0.39%, or 0.59% tryptophan. After 14 weeks, feed intake was depressed in fish fed the diets containing 0.06% or 0.16% tryptophan. No further differences in feed intake were noted between the remaining treatments. In addition, body weight was lower in fish fed diets containing 0.06%, 0.16%, or 0.21% tryptophan compared with fish fed higher levels. After 16 weeks of feeding the test diets, plasma tryptophan levels were found to be directly related to dietary tryptophan levels. Similarly, increased dietary levels of tryptophan resulted in increased brain levels of tryptophan, serotonin, and 5-hydroxyindoleacetic acid. These results demonstrate that in rainbow trout, as in mammals, altered dietary levels of tryptophan result in alterations in plasma and brain tryptophan, brain serotonin, and brain 5-hydroxyindoleacetic acid.

Fenfluramine-induced behavior changes in rats prefed serotonin-altering amounts of tryptophan and pyridoxine

It has been well established that elevated dietary tryptophan (TRP) levels can increase brain serotonin concentrations, thereby influencing serotonergic transmission. We previously examined interaction between dietary substrate (TRP: 0.15 and 0.6%) and the cofactor precursor (pyridoxine HCl: 3 and 3,000 mg/kg) on brain serotonin metabolism, observing significant increases in serotonin concentrations from such dietary interaction. The present experiments were designed to explore possible behavioral consequences of the substrate-cofactor interaction. After the IP injection of fenfluramine (FA: at 5, 10, 15, and 20 mg/kg), serotonin-mediated behavior traits and the appearance of flushing were observed in rats fed experimental diets as stated above. With a 5 mg/kg dose of FA, a differential dietary effect was most visible. However, at higher FA levels (15 and 20 mg/kg), such dietary effects were no longer discernible. The appearance of flushing was also dependent on dietary TRP intake and the dosage of FA. These results indicate a clear substrate-cofactor interaction on certain serotonin-mediated behavior traits in the rat.

Effects of dietary tryptophan levels on growth, feed/gain, carcass composition and liver glutamate dehydrogenase activity in rainbow trout ( Salmo gairdneri)

1. 1. The tryptophan requirement of rainbow trout (initial body wt, 13 g) was estimated by feeding diets containing varied levels of tryptophan from 0.06 to 0.5% of diet for 6 weeks. 2. 2. The estimated tryptophan requirement was 0.20–0.25(0.57–0.71)% of diet (dietary protein). 3. 3. Nitrogen retention increased and feed/gain decreased with dietary tryptophan levels up to 0.14%, but no further effect was observed at levels above 0.14%. 4. 4. Carcass protein content gradually increased and lipid and ash contents decreased with increasing dietary tryptophan levels. 5. 5. Dietary tryptophan levels did not affect hepatosomatic index or liver glutamate dehydrogenase activity.

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.

Tryptophan requirement of laying hens.

1. In order to determine the tryptophan requirement of laying hens, 4 experiments were conducted. Single Comb White Leghorn hens older than 15 months were supplied diets with graded levels of tryptophan from 0.086 to 0.32 % ad libitum.2. The egg production rate (Y1, %) changed according to the equation Y1=3.2+0.816X-0.00194X2, where X represents mg of daily tryptophan intake/hen. The maximal 89.0% of egg production rate was obtained at 210 mg tryptophan intake/hen/day.3. The egg production (Y2, g/hen/day) changed according to the equation Y2=5.3+0.476X-0.00110X2. The maximal 54.9 g/hen/day of egg production was obtained with an intake of 212 mg tryptophan per hen daily.4. The equation of the response of food intake (Y3, g/hen/day) was Y3=3.9+0.687X-0.00162X2. The point at which the daily food intake was maximized (111.6g) was computed to be 212 mg tryptophan intake/hen/day.5. The dietary tryptophan level which maximized the egg production rate, egg production and food intake was calculated to be 0.189%.6. Plasma tryptophan concentrations increased with dietary tryptophan intakes and then reached a plateau at 191 mg tryptophan intake/hen/day.

Tryptophan Requirement of the 2.5-kg Piglet Determined by the Oxidation of an Indicator Amino Acid

The tryptophan requirement of 2.5-kg piglets was measured by the oxidation of L-[1-14C]phenylalanine or DL-[1-14C]lysine when meals containing various levels of L-tryptophan were offered. Increasing dietary tryptophan from 0.65 to 2.0 g/kg decreased 14CO2 release from L-[1-14C]phenylalanine but further increases in dietary tryptophan level resulted in no further decrease in 14CO2 output. Regression analysis, with a crossover model, showed phenylalanine oxidation was minimized with a dietary tryptophan level of 1.94 g/kg (95% confidence limits 1.93 to 1.95). The oxidation of lysine was also reduced by increasing tryptophan levels to 2 g/kg; as tryptophan level was increased to 3 g/kg there was no statistically significant reduction of lysine oxidation. These studies suggest that the dietary tryptophan requirement of the 2.5-kg piglet is no more than 2 g/kg of a 240 g protein per kilogram diet.

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.

Effect of Tryptophan Intake on Oxidation of [7a-14C]Tryptophan and Urinary Excretion of N1-Methylnicotinamide in the Rat

Oxidation of tryptophan and urinary excretion of niacin metabolites were studied in weanling rats fed ad libitum for 12 to 16 days niacin-free and nicotinamide-supplemented (20 mg/kg of diet) diets containing 15% of crystalline amino acids and from 0.04 to 1.0% of l-tryptophan. N1-methylnicotinamide was measured in urine collected during the last 3 days of the feeding period. After the feeding period, rats were placed in metabolic cages, and each rat was given 4 g (dry weight) of diet containing a tracer dose of dl-[7a-14C]tryptophan. Expired CO2 was collected hourly for 10 hours. In both the niacin-free and nicotinamide-supplemented groups, weight gains increased with increasing increments of tryptophan up to about 0.16% l-tryptophan. With more than 0.16% of l-tryptophan, the amount of N1-methylnicotinamide excreted per day by both groups of rats increased linearly with increasing tryptophan intake, but proportionately less N1-methylnicotinamide was excreted when the dietary tryptophan level was 1.0%. The amount of tryptophan oxidized per 10 hours increased linearly with increasing dietary tryptophan levels between 0.16 and 1.0%. Therefore, the decline in excretion of N1-methylnicotinamide with the 1.0% tryptophan level could not be accounted for by increased oxidation. These results suggest that after the tryptophan requirement for growth is met, the amount of tryptophan oxidized and converted to nicotinamide is directly proportional to the level of tryptophan intake up to about 3 times the requirement for growth. The tryptophan requirement of the growing rat fed niacin-free and nitcotinamide-supplemented diets estimated from the inflection points of N1-methylnicotinamide excretion curves was in good agreement with the requirement of about 100 µmoles/day determined from the growth curve.amino acid oxidation tryptophan niacin niacin formation from tryptophan

Histidine, phenylalanine-tyrosine and tryptophan requirements for growth of the young kitten.

Growth assays were conducted to estimate the minimal dietary requirement levels of histidine, tryptophan, phenylalanine and tyrosine for the young kitten. Dietary concentrations of histidine and tryptophan of .30 and .15%, respectively, were found to support optimal kitten performance. A preliminary study of the total aromatic amino acid (TAAA) requirement indicated that no more than 1.20% TAAA (.60% phenylalanine + .60% tyrosine) is required by the kitten. Subsequent experiments revealed no decrease in growth rate when TAAA were reduced to 1.00% of the diet. At this level of TAAA, tyrosine could supply 50% of the requirement for TAAA.

Dietary tryptophan level and the enzymes of tryptophan NAD pathway.

1. Dietary tryptophan was found to regulate the activities of tryptophan oxygenase (EC 1.13.1.12) and quinolinate phosphoribosyltransferase (EC 2.4.2a) in liver. 2. With increasing tryptophan concentration in the diet containing 100 g protein/kg, tryptophan oxygenase activity increased while that of quinolinate phosphoribosyltransferase decreased. The response of these enzymes to dietary tryptophan at lower dietary protein level (25 g/kg) was not significant. 3. Liver nicotinate phosphoribosyltransferase (EC 2.4.2.11) activity and kidney picolinate carboxylase (EC 4.1.1.45) activity were unaltered with different tryptophan concentrations in the diet. 4. The response of various biochemical measurements was dependent on the tryptophan intake and the changes were marked below and above the requirement level of tryptophan. 5. It is suggested that the urinary excretion of quinolinic acid and N'-methylnicotinamide may be useful in assessing the tryptophan nutritional status and its requirement.

Evaluation of Dietary Tryptophan Levels as a Restriction Method for Broiler Breeder Pullets , ,

A total of 2,000 pullets and 300 cockerels from a broiler strain were started on experiment at two weeks of age. The following treatments were used: (1) 0.150 percent tryptophan and 28 mg. added niacin per kg. of diet; (2) 0.150 percent tryptophan and no added niacin in the diet; (3) 0.150 percent tryptophan with 28 mg. added niacin per kg. of diet; (4) 0.125 percent tryptophan with 28 mg. added niacin per kg. of diet; and (5) 0.100 percent tryptophan with 28 mg. added niacin per kg. of diet. Treatment 1 was limited daily, the others were ad libitum. Birds were maintained on these treatments until 22 weeks of age, at which time they were moved to a breeder house. During the breeder phase, the birds were subjected to either of two treatments; a constant protein level program or a two protein level phase feeding program.Body weights at 22 weeks of age were reduced by decreasing tryptophan levels. However, percent body fat increased with lower levels of tryptophan. Birds on low tryptophan levels consumed less feed per bird per day but feed efficiency was increased. Body weight increased greatly in Treatment 5 birds during the breeder phase. Hen day production and hen housed production were reduced in those previously fed the low levels of tryptophan. Hatch of total eggs set was also reduced by the lowest level of tryptophan; however, hatch of fertile eggs was not affected. Limited fed birds performed better overall in the breeder house than ad libitum fed birds.

The association between colorectal cancer and breast cancer

Evidence for an association between colorectal cancer and breast cancer is reviewed. Consistent with a dietary hypothesis to account for a relationship between the cancer sites, intestinal and breast cancers show a similar pattern in correlations of cancer mortality and incidence rates with per capita food consumption figures. The international data indicate that meat, particularly cattle meat, is the food most closely associated with both colorectal and breast cancer rates. In the one case-control study which has shown dietary factors to be related to colorectal cancer [1], the specificity of beef as the most suspect food item implied the need for studies of long-chain, saturated fatty acids. A high animal fat and protein diet could also mean elevated levels of dietary tryptophan. Studies of tryptophan metabolism are viewed as suggestive of a biochemical mechanism for the interaction of nutritional and hormonal factors. A hormonal mechanism affected by dietary fat has similarly been postulated [2] and has some experimental support [3]. Possible research in further exploration of an association between colorectal and breast cancers is suggested.

The Effect of Dietary Tryptophan and Niacin Levels on Broiler Breeder Pullets ,

A total of 1500 pullets and 300 cockerels were obtained at one-day of age and reared to six weeks of age on a commercial-type diet. At six weeks of age, birds were fed one of the following: Diets 1, 2 and 3 contained 0.150 percent tryptophan and no added niacin, 28 mg. added niacin and 280 mg. added niacin per kg. of diet, respectively. Diets 4, 5 and 6 contained 0.112 percent tryptophan and no added niacin, 28 mg. added niacin and 280 mg. added niacin per kg. of diet, respectively. All diets contained 2800 kcal. of metabolizable energy per kg. of diet and were fed for 21 weeks.The 0.112 percent tryptophan diets reduced body weight and percent body protein but increased percent body fat. Niacin levels had no effect on any of the pullet production parameters measured. However, at 21 weeks of age 280 mg. of added niacin in the 0.150 percent tryptophan diets restricted body weights of the males.

PERFORMANCE OF CHICKS FED GRADED LEVELS OF NIACIN AND TRYPTOPHAN

The effect of excess dietary niacin on the performance of chicks was investigated in a factorial experiment in which niacin and tryptophan were studied simultaneously in terms of interdependence. Weight gain of chicks was increased with increasing levels of dietary tryptophan. Dietary supplementation of niacin enhanced feed consumption, thus resulting in significant weight gain but excess dietary niacin appeared to depress feed consumption and hence retard chick growth. Tryptophan was observed to partially spare dietary niacin but could not compensate entirely for a niacin deficiency. It is concluded that the maximum dietary requirement of niacin is no higher than 30 mg/kg of feed at any level of tryptophan, and that any additional input of the vitamin may negatively affect feed consumption and weight gain of the chicks.

Tryptophan Intake, Spacing of Meals, and Diurnal Fluctuations of Plasma Tryptophan in Men

The influence of adequate and low tryptophan intakes and the spacing of meals on the concentration of tryptophan in blood plasma of normal adult men was examined. For both levels of dietary tryptophan, when four meals were given daily, at 8:00 AM, 12:00 noon, 4:00 PM, and 9:00 PM, the plasma tryptophan level rose between 1:00 AM and 8:00 AM and decreased between 8:00 AM and 12:00 noon. Plasma tryptophan concentration did not increase in the early morning hours when six meals were offered at 4-hr intervals throughout the day.

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.

Effect of Varying Levels of DL-Tryptophan in Diet on Dental Caries in Rats.

SummaryDental caries experience in rats was studied following feeding of varying levels of DL-tryptophan as a constituent of a cariogenic diet. When either 0.6 or 1.8 g/kilo tryptophan was added to the diet there was an increase in dental caries, although the differences were not significant. When the diet contained 5.4 g/kilo tryptophan there was a significant increase in incidence of dental caries. Concomitant with the increased dietary tryptophan level, there was an increased salivary tryptophan concentration.

Liver pyridine nucleotide content as related to dietary tryptophan and nicotinic acid in the chick

There is no correlation between liver pyridine nucleotide level and growth rate. At normal dietary levels of tryptophan and niacin, the former contributes more to the storage of pyridine nucleotides in the liver. At equimolar levels of feeding, niacin is more efficient than tryptophan in increasing the storage of liver pyridine nucelotides.