Histidine Articles 2

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Effects of Thiamine and Riboflavin Deficiency on Histidine Metabolism

         (Baldridge 1958) Download

Histidine metabolism in the human adult: histidine blood tolerance, and the effect of continued free L-histidine ingestion on the concentration of imidazole compounds in blood and urine

            (Block, Westhoff et al. 1967) Download

Histidine-stimulated acid secretion in the conscious rat is mediated by amino acid uptake system N

            (Dimaline, Wilkinson et al. 1990) Download

The characteristics of sodium-dependent, histidine-stimulated gastric acid secretion were studied in the conscious gastric-fistulated rat. Intragastric L-histidine, but not glutamine, asparagine, glutamic acid or glycine, stimulated acid secretion. The histidine-stimulated acid secretion was inhibited by the presence of glutamine or asparagine, but not by glutamic acid or glycine. The substitution of lithium for sodium in the gastric perfusate was tolerated. Together with previous data, the results indicate that an N-like amino acid uptake system mediates histidine-stimulated acid secretion in the conscious rat.

Enhancement of histidine and one-carbon metabolism in rats fed high levels of retinol

            (Fell and Steele 1982) Download

Histidine metabolism was studied in rats fed 10% casein diets supplemented with 1000 IU of retinol/g concurrent with or previous to exposure to high levels of dietary histidine (1% or 2%). When a retinol-supplemented 10% casein + 1% histidine diet was fed ad libitum for 21 days, urinary excretion of formiminoglutamic acid (FIGLU) was decreased by 50-70% over the entire period and plasma histidine was reduced by 30-70% for 16 days compared to rats receiving 10% casein + 1% histidine with normal levels of retinol. Rats pretreated for 10 days with a 10% casein diet supplemented with high levels of retinol oxidized 30% more L-[ring-2-14C]histidine to 14CO2 and excreted 76% less of the administered dose as urinary FIGLU compared to control rats not pretreated with high levels of retinol. Depression in growth due to supplementation of a 10% casein diet with 1% histidine were also partially alleviated in rats that were first pretreated with retinol. Activities of histidase, urocanase, and formiminoglutamic acid formiminotransferase (FIGLU transferase) were unaffected by retinol supplementation. The results suggest that retinol supplementation enhances histidine catabolism by exerting a change on one-carbon metabolism.

Effect of histidine intake of plasma and urine histidine levels, nitrogen balance and N tau-methylhistidine excretion in normal and chronically uremic men

            (Kopple and Swendseid 1981) Download

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. N tau-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.

Long-term effects of histidine depletion on whole-body protein metabolism in healthy adults

            (Kriengsinyos, Rafii et al. 2002) Download

The essentiality of histidine in healthy adults is a controversial topic. To study the potential metabolic effects of a lack of exogenous histidine, four healthy adults consumed a histidine-free diet, with adequate energy and 1.0 g/(kg. d) of an L-amino acid mixture for 48 d. Protein metabolism was monitored every 4 d by using indicator amino acid (L-[1-(13)C]phenylalanine) oxidation (in four subjects) and [(15)N]glycine (in one subject). Urine samples (24-h) were collected for measurement of urea, total nitrogen, creatinine, 3-methylhistidine (3-MH), histidine and beta-alanine. Albumin, transferrin and hematologic concentrations were measured on d 0, 24 and 48. Urinary excretion of nitrogen, urea, creatinine and 3-MH were not affected by the histidine-free diet. However, there was a significant (P < 0.001) linear decline (24-28%) in whole-body protein turnover. Significant (P < 0.05) decreases in albumin (12%), transferrin (17%) and hemoglobin (Hb) (11%) concentrations occurred slowly over the histidine depletion period. The urinary excretion of beta-alanine (an index of carnosine catabolism) generally increased in the smallest subject during the consumption of histidine-free diet. This study demonstrates that a lack of histidine in the diet for a prolonged period resulted in an accommodation of protein turnover and phenylalanine oxidation, measured by the (13)C-phenylalanine indicator amino acid. The extensive metabolic accommodation, together with decreases in Hb, albumin and transferrin during histidine depletion, leaves unresolved the issue of whether histidine is a dietary essential amino acid in healthy adults.

Peptide Histidine Valine-42 Stimulates Gastric Acid Secretion in Man

         (Nikou, Yiangou et al. 1989) Download

The effect of peptide histidine valine-42 (PHV-42) on gastric acid secretion was studied in man. PHV-42 was infused into 5 healthy volunteers at a dose of 10 pmol/kg/min. This dose caused a significant stimulation of basal gastric acid and potassium output. There were no significant changes in circulating gastrin throughout the infusion. In 2 subjects with a background of submaximal pentagastrin stimulation, PHV-42 infusion at the same dose did not alter acid secretion in either subject. The previous observation that PHV-42 is found particularly in the stomach and the new finding that it stimulates basal gastric secretion suggest the possibility that PHV-42 could have a role in local control of acid secretion.

Gastric secretion

            (Schubert 2001) Download

The influence of central and peripheral stimuli on gastric acid secretion is mediated via activation of histaminergic, gastrinergic, and cholinergic pathways coupled to intracellular second-messenger systems that determine the trafficking and activity of H+ K+-ATPase, the proton pump of the parietal cell. Histamine, released from enterochromaffin-like cells stimulates the parietal cell directly via H-2 receptors coupled to generation of cAMP. Gastrin, acting via cholecystokinin-2 receptors on enterochromaffin-like cells coupled to an increase in intracellular calcium, stimulates the parietal cell indirectly by activating histidine decarboxylase, releasing histamine, and inducing enterochromaffin-like cell hypertrophy and hyperplasia. Acetylcholine, released from gastric postganglionic intramural neurons, stimulates the parietal cell directly via M-3 receptors coupled to intracellular calcium release and calcium entry. The second-messenger systems activated in the parietal cell converge on H+ K+-ATPase that catalyzes the exchange of luminal K+ for cytoplasmic H+ and is responsible for gastric luminal acidification. The main inhibitor of acid secretion is somatostatin which, acting via sst2 receptors, exerts a tonic inhibitory influence on parietal, enterochromaffin-like, and gastrin cells. Acute infection with Helicobacter pylori results in hypochlorhydria, whereas chronic infection may be associated with either hypo- or hyperchlorhydria. Although prostaglandins are thought to play a physiologic role in the regulation of acid secretion and maintenance of gastric mucosal integrity, the precise roles of cyclooxygenase-1 and cyclooxygenase-2 in these processes still eludes us.


References

Baldridge, R. C. (1958). "Effects of thiamine and riboflavin deficiency on histidine metabolism." J Nutr 66(1): 29-34.

Block, W. D., M. H. Westhoff, et al. (1967). "Histidine metabolism in the human adult: histidine blood tolerance, and the effect of continued free L-histidine ingestion on the concentration of imidazole compounds in blood and urine." J Nutr 91(2): 189-94.

Dimaline, R., M. Wilkinson, et al. (1990). "Histidine-stimulated acid secretion in the conscious rat is mediated by amino acid uptake system N." Exp Physiol 75(5): 717-20.

Fell, D. and R. D. Steele (1982). "Enhancement of histidine and one-carbon metabolism in rats fed high levels of retinol." J Nutr 112(3): 474-9.

Kopple, J. D. and M. E. Swendseid (1981). "Effect of histidine intake of plasma and urine histidine levels, nitrogen balance and N tau-methylhistidine excretion in normal and chronically uremic men." J Nutr 111(6): 931-42.

Kriengsinyos, W., M. Rafii, et al. (2002). "Long-term effects of histidine depletion on whole-body protein metabolism in healthy adults." J Nutr 132(11): 3340-8.

Nikou, G. C., Y. Yiangou, et al. (1989). "Peptide histidine valine-42 stimulates gastric acid secretion in man." Biosci Rep 9(3): 369-74.

Schubert, M. L. (2001). "Gastric secretion." Curr Opin Gastroenterol 17(6): 481-8.