Dietary Histidine Research Articles

Effect of dietary histidine on histidine-catabolizing enzymes in the chicken ( Gallus domesticus)

Experiments were conducted to determine the influence of dietary histidine on histidine catabolism in the chick and to determine possible nutritional interrelationships between histidine and potassium salts of metabolizable organic anions. Supplemental histidine (5.5–6.0%) decreased weight gain and food consumption of chicks, increased liver size, and doubled the activities of liver histidase (EC 4.3.1.3) and histidine-pyruvate aminotransferase (EC 4.2.1.49). Histidine depressed plasma potassium concentration; no other interaction of potassium and histidine was observed.

Experience and Problems of Newborn Mass Screening for Inborn Errors of Metabolism in Japan

Summary A program of newborn mass screening for inborn errors of metabolism has since 1977 been conducted by The Ministry of Health and Welfare in Japan with great success in preventing mental and physical handicaps in children and estimating the incidence of these diseases in our country as follows: phenylketonuria (PKU) 1/78,100 maple syrup urine disease (MSUD) 1/281,200 histidinemia 1/10,600 galactosemia 1/156,200 There are some genetic variants of each of these diseases, PKU, MSUD and others. Circumspection is therefore required in making a diagnosis or selecting a particular method of treatment. When MSUD is suspected, it is necessary to make a definite diagnosis promptly and take therapeutic measures including peritoneal dialysis. The efficacy of low histidine diet in histidinemia is not yet ascertained. Close inquiries should be made about the benefit of such a dietary regimen and the long term prognosis therewith. A screening test for homocystinuria by the detection of blood methionine level is difficult. In cases with high blood methionine level during the neonatal period, it is necessary to differentiate the condition from other disease with high blood methionine. Hepatorenal tyrosinemia appears to be unsuitable for mass screening because of the the unefficacy of low phenylalanine tyrosine diet in some of the patient and the difficulty to differentiate from transient tyrosinemia in normal newborn infants. However, mass-screening is recommendable for Richner-Hanhalt type tyrosinemia which responds well to dietary therapy and which is easy to differentiate from the transient tyrosinemia because of the marked elevation of blood tyrosine.

Effect of Histidine Intake on Plasma and Urine Histidine Levels, Nitrogen Balance and N7-Methylhistidine Excretion in Normal and Chronically Uremic Men

This study assessed whether changes in plasma histidine or nitrogen balance could indicate the dietary histidine requirement in short-term feeding studies. Five normal and two chronically uremic men were fed diets varying in histidine content in a metabolic research unit. Subjects received amino acid diets for 71 ± 12 (sd) days during which time the histidine intake was varied between 60 and 2,800 mg/day at 8.0 ± 0.5 day intervals. The results indicated that both postabsorptive plasma histidine and urinary histidine correlated with the dietary histidine intake. However, in individual patients the response curve of plasma histidine to the dietary histidine intake did not demonstrate a consistent breakpoint which could be used to indicate the dietary histidine requirement. Rather, the histidine intake above which the plasma levels increased rapidly seemed to be influenced by the previous dietary histidine. Urinary histidine excretion also correlated with plasma histidine. N7-methylhistidine was increased in plasma and reduced in urine of the uremic patients as compared to normal subjects. Nitrogen balances were less positive with histidine intakes of 2 mg/kg/day or lower. These data support the finding that histidine is an essential amino acid in normal and chronically uremic man. However, clinical and metabolic studies of greater duration may be necessary to determine the daily histidine requirement.histidine essential amino acids nitrogen balance 3-methylhistidine

Influence of dietary histidine on tissue histamine concentration, histidine decarboxylase and histamine methyltransferase activity in the rat.

Three-week-old male rats were fed for two weeks diets supplying inadequate, adequate, or excess amounts of histidine. After the 2-week feeding of the experimental diets, the rats were killed. Brain, gastrocnemius muscle, kidney and stomach were removed and analyzed for histamine and free-histidine as well as for the degradative enzyme, HMT, and the histamine-synthesizing enzyme HDC. The following results were obtained: As the levels of dietary histidine increased, (1) tissue concentrations of free-histidine and of histamine increased in all the tissues analyzed. (2) The increase of histamine was greatest in brain and stomach (5- and 4-fold, respectively), but less in kidney and muscle (2-fold). (3) HDC activity was not detected in muscle, but doubled from the lowest to the highest histidine intake in brain and increased almost 6-fold between the lowest and the highest histidine levels in stomach. (4) Kidney HDC decreased from the lowest to the two higher levels of dietary histidine. (5) HMT activity increased nominally in brain and not significantly in kidney; none was detected in either muscle or stomach. (6) Brain and kidney, tissues with considerable HMT activity, had almost no histamine. The increases in tissue histamine concentrations observed in the tissues analyzed generally reflected the changes and magnitudes of enzyme activities for HMT and HDC. The results in the rat differ in important ways from those previously observed in chickens as follows: (1) Histamine concentrations as a function in dietary histidine decreased in the chick. (2) Both HDC and HMT activities were present in chick muscle tissue. (3) HDC activity in chick stomach decreased sharply as a function of dietary histidine.

Leucine, Isoleucine, Valine and Histidine Requirements of Fingerling Channel Catfish

Growth studies were conducted with fingerling channel catfish to determine the minimal requirements for the amino acids leucine, isoleucine, valine and histidine. The experimental diets were formulated from purified ingredients to contain 24% crude protein and 275 kcal/100 g diet. Casein and gelatin served as protein sources and were supplemented with crystalline L-amino acids to provide the amino acid pattern found in 24% crude protein from whole egg powder. Based on dry diet the catfish required 0.84 +/- 0.04% leucine, 0.62 +/- 0.04% isoleucine, 0.71 +/- 0.03% valine and 0.37 +/- 0.01% histidine. These values correspond to 3.50% leucine, 2.58% isoleucine 2.96% valine and 1.54% histidine when expressed as a percentage of dietary protein. Quantitation of serum free amino acid levels revealed a marked increase in valine and isoleucine in leucine-deficient fish. In addition, increases in dietary isoleucine or valine resulted in changes in the serum levels of isoleucine, valine and leucine. These data indicate an apparent interaction among these amino acids in the catfish comparable to that previously observed in other species. Dietary histidine caused no increase in serum free histidine levels until the dietary requirement was reached. Muscle carnosine could not be detected in the catfish.

Effect of age and dietary histidine on histamine metabolism of the growing chick.

The effect of age and of varying the dietary histidine level, with special emphasis on histamine metabolism, was studied in male, white Leghorn chicks. The birds were fed a 19% amino acid diet with histidine supplied from 0 to 0.8% of diet. In Experiment 1, 7-day-old chicks were fed the experimental diets for 7 days. In Experiment 2, chicks were fed the experimental diets for different time intervals to equalize their body weight at time of killing. In Experiment 3, birds were killed at 5, 9, 12 and 15 days of age when their body weights reached 69, 96, 136 and 184 g, respectively. Concentrations of anserine, carnosine, free-histidine and histamine, and activities of histidine decarboxylase (HDC) and histamine methyl transferase (HMT) were assayed in whole brain, pectoralis major muscle and in proventriculus of 3 or 4 chicks per treatment group.

Effect of Dietary Histidine on Tissue Concentrations of Histidine-containing Dipeptides in Adult Cockerels

Effect of Dietary Histidine on Tissue Concentrations of Histidine-containing Dipeptides in Adult Cockerels

Developmental Changes and Dietary Histidine Manipulation: Effect on Rat Olfactory Bulb and Leg Muscle Components

Developmental Changes and Dietary Histidine Manipulation: Effect on Rat Olfactory Bulb and Leg Muscle Components

Effects of dietary histidine and arginine on plasma amino acid and urea concentrations of men fed a low nitrogen diet

The effects of dietary histidine and arginine on fasting and 1 and 2 hour postprandial plasma free amino acid and urea concentrations were studied in six young men. For 1 week each, they were fed six different diets containing 6.3 g of nitrogen daily. Each diet contained eight indispensable amino acids, cystine and tyrosine proportioned as in casein and a different mixture of dispensable nitrogen: A) six dispensable amino acids plus argine (diet 1) or plus histidine and arginine (diet 2) in the casein pattern, or B) an isonitrogenous amount of glycine and diammonium citrate alone (diet 3), with histidine (diet 4), with arginine (diet 5) or with histidine and arginine (diet 6). The fasting plasma concentrations of the seven indispensable amino acids assayed and their similar postprandial patterns were unaffected by the dietary treatments. Both fasting and postprandial plasma histidine concentrations were significantly lower when the histidine-low diets were fed than when the histidine-supplemented diets were fed. Histidine supplementation promoted a reduction in fasting plasma urea nitrogens. Proline concentrations were lowered significantly when proline was removed from the dietary amino acid mixtures, but plasma arginine concentrations were unaffected by arginine removal. Plasma histidine was maintained at lower concentrations in dietary histidine deficiency than when histidine was added to the low nitrogen diets.

Effects of Dietary Histidine and Arginine on Nitrogen Retention of Men

Effects of dietary histidine and arginine on nitrogen retention were compared in six young men consuming for 1 week, each of six semipurified diets containing eight indispensable amino acids proportioned as in casein and 6.3 g nitrogen daily. Nonspecific nitrogen was either A) a mixture of six dispensable amino acids and arginine (diet 1) or arginine and histidine (diet 2) in casein proportions, or B) an isonitrogenous mixture of glycine and diammonium citrate alone (diet 3), with histidine (diet 4), arginine (diet 5), or histidine and arginine (diet 6). Nitrogen retention was significantly greater when the nonspecific nitrogen source was dispensable amino acids, arginine and histidine (diet 2) than when it was glycine and diammonium citrate (diet 3). mean balances were positive only when diets contained histidine (diets 2, 4, and 6). Histidine with arginine (diets 2 and 6) significantly improved nitrogen retention compared to arginine alone, but the balance, although positive, was not significantly improved when histidine was fed without arginine (diet 4). Urinary urea nitrogen confirmed these data. Indicators of erythrocyte status, plasma enzyme activities and proteins, and creatinine clearance were unaffected by diet. In summary, histidine supplementation of the low nitrogen diet improved total nitrogen utilization when arginine was present in the diet.

Effect of Dietary Histidine Deprivation in Two Rat Strains on Hemoglobin and Tissue Concentrations of Histidine-containing Dipeptides

Effect of Dietary Histidine Deprivation in Two Rat Strains on Hemoglobin and Tissue Concentrations of Histidine-containing Dipeptides

Effect of Histidine Intake and Hepatic Histidase Activity on the Metabolism of Histidine in Vivo

The metabolic fate of histidine was investigated in young male rats fed diets containing from 0 to 0.6% of L-histidine and 14.7% of a mixture of other L-amino acids. Liver histidase activity was not influenced by dietary histidine content. Tissue histidine concentration increased gradually, then more sharply, as dietary histidine content was increased from 0 to 0.325% then it plateaued. During ad libitum consumption of these diets containing L-[U-14C]histidine, 14CO2 production remained low until dietary histidine content exceeded 0.25%, then it increased linearly until with 0.6% of dietary histidine 25% of the absorbed dose was oxidized. The proportion of absorbed 14C incorporated into tissue proteins was high when dietary histidine content was low and decreased as dietary histidine content increased. Histidine requirement estimated from the inflection point of the oxidation curve was in good agreement with values determined from growth response and urinary nitrogen excretion. Liver histidase activity increased almost linearly with increasing dietary casein content. Rats fed 12% casein oxidized more of a load of L-[ring-2-14C]histidine (500 mg/100 g rat) to CO2 than those fed 8% casein. Plasma histidine clearance rate after intraperitoneal injection of 50 mg histidine/100 g rat increased as the casein content of the diet was increased from 4% to 8%, 12% and 40%.

The effects of dietary histidine, methionine and homocystine on vitamin B12 and folate levels in rat liver.

1. L-histidine (20 g/kg) added to vitamin B12-deficient and cyanocobalamin-supplemented diets based on soya-bean flour reduced the growth of rats given the vitamin B12-deficient diet but stimulated growth of rats given the cyanocobalamin-supplemented diet. Liver weight (g/kg body-weight)increased, but the protein content of the livers decreased, in rats given histidine supplements. The histidine was associated with significantly higher folate concentrations in the livers of cyanocobalamin-supplemented rats.

Evidence that histidine is an essential amino acid in normal and chronically uremic man.

The requirement for dietary histidine was investigated in four normal and three chronically uremic men. Subjects lived in a metabolic unit where they were fed three isonitrogenous diets in the following order: a 40-g protein diet (28 plus or minus SD 8 days), a semi-synthetic amino acid diet deficient in histidine (35 plus or minus 2 days), and an amino acid diet which contained histidine (31 plus or minus 5 days). With ingestion of the histidine-deficient diet, nitrogen balance gradually became negative, and serum albumin decreased in six subjects. Plasma histidine fell by 82 plus or minus 6 per cent; muscle histidine decreased by 62 plus or minus 19 per cent; the hematocrit fell by 25 plus or minus 9 per cent; and serum iron rose. Subjects felt unwell, and in five cases a skin lesion consisting of fine scales, dry skin, and mild erythema developed. After administration of the histidine-repletion diet, nitrogen balance became positive in six subjects; serum albumin increased in five cases; plasma and muscle histidine rose; serum iron fell abruptly; a reticulocytosis ensued; and the hematocrit rose. The clinical symptoms and skin lesions disappeared. These observations indicate that histidine is an essential amino acid in normal and chronically uremic man. The absence of dietary histidine is associated with failure of normal erythropoiesis.

Histidinemia produced in the rat by treatment with nitromethane1.

Metabolic effects of in vivo administration of nitromethane, a histidase inhibitor, were studied in the rat. Histidinemia produced by feeding a 5-percent histidine diet to the rat was included for comparison. Rats injected subcutaneously with nitromethane every other day appeared to be histidinemic, with a plasma histidine level of 43 mumol/100 ml (control 9.2 mumol/100 ml) after 12 days of treatment. Histidine concentrations in the brain, liver, kidney, and urine of the nitromethane-treated rats were also increased. Liver histidase activity was decreased about 78 percent after nitromethane administration, and the rate of in vivo CO2 production from histidine was also depressed. No abnormal change in liver and kidney sizes was observed in these animals. Rats fed the 5-percent histidine diet showed markedly higher plasma histidine concentrations (99 mumul/100 ml) than the nitromethane-treated rats. The magnitude of increase in plasma histidine in the histidine-fed rats was considerably greater than that observed in humans with histidinemia. Furthermore, the liver histidase activity was decreased only by about 20 percent, and a significant increase in liver and kidney sizes was noted in the histidine-fed animals. These findings indicate that histidinemia produced by nitromethane administration is a better model for studies of the genetic disorder than histidinemia induced by high levels of histidine in the diet.

Alleviation of parakeratosis in zinc deficient swine by high levels of dietary histidine.

Alleviation of parakeratosis in zinc deficient swine by high levels of dietary histidine.

Plasma and tissue cholesterol and lipid levels in rabbits on L-histidine-supplemented diets.

SummaryFeeding 5 and 8% excess L-histidine to rabbits caused significantly elevated plasma cholesterol levels. Phospholipid levels were slightly but not significantly elevated. The 5% histidine-supplemented diet produced plasma levels of 20–50 mg/100 ml of histidine. After 17 weeks on diet, no effects on brain cerebrum and cerebellum or liver cholesterol concentrations were found. Brain and liver total lipid and phospholipid and cerebrum galactolipid concentrations were also normal. The effect of excess dietary histidine on lipid components is apparently localized in the circulatory system. The effects noted in rabbits are much less than those previously observed in monkeys.The technical assistance of Robert Colwell and Robert Jaeger was greatly appreciated.

Cellular transport of L-histidine in Hartnup disease.

The urinary excretion, the intestinal absorption, and the elimination of histidine from blood were studied in two patients with Hartnup disease. On standard diet the patients lost a great proportion of the dietary histidine in the urine, whereas the fecal loss was negligible. A high oral dose of L-histidine gave only a slight increase in plasma histidine and no increase in fecal histidine, but a considerable increase in the urinary histidine output. Intravenously administered L-histidine was eliminated more rapidly than in controls. The lack of increase in plasma histidine after the oral loading may be explained by the rapid elimination from the blood. This was mainly due to a rapid cellular uptake of histidine which is supposed to be a normal reaction of histidine-deprived cells. Thus the only obvious defect in the histidine transport in Hartnup disease is the reabsorption defect in the renal tubules. A generally impaired cellular transport of L-histidine is improbable.

Quantitative dietary requirements for histadine in the saw-toothed grain beetle, Oryzaephilus surinamensis (L.) (coleoptera, silvanidae)

1. 1. Histidine is essential in the diet of Oryzaephilus surinamensis (L.), the optimal concentration being between 2·0 and 4·0 mg/g of diet. 2. 2. Concentrations of dietary histidine of 5·0 and 6·0 mg/g were harmful the larvae. 3. 3. Addition of equimolecular amounts of glycine to maintain the diet isonitrogenous when histidine concentrations were reduced was harmful to the larvae. 4. 4. Histidine could not be replaced in the diet for O. surinamensis by additional quantities of guanine.

The effect of dietary histidine and arginine on growth in the guinea-pig as a test of the amino acid imbalance in plantain and cassava

We have studied guinea-pig growth curves, using diets that highlight amino acid imbalance in staple foodstuffs used in Africa. Histidine (high in plantain) added to normal guinea-pig diets improved growth performance; histidine or arginine (high in cassava) added to low protein diets depressed growth.