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Relevant bibliographies by topics / Urinary tryptophan

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Academic literature on the topic 'Urinary tryptophan'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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Journal articles on the topic "Urinary tryptophan"

1

Oshima, Shiiya, and Nakamura. "Combined Supplementation with Glycine and Tryptophan Reduces Purine-Induced Serum Uric Acid Elevation by Accelerating Urinary Uric Acid Excretion: A Randomized, Single-Blind, Placebo-Controlled, Crossover Study." Nutrients 11, no. 11 (2019): 2562. http://dx.doi.org/10.3390/nu11112562.

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The authors previously confirmed the serum uric acid-lowering effects of the combination of glycine and tryptophan in subjects with mild hyperuricemia. This study examined whether combined supplementation with glycine and tryptophan suppressed the elevation in serum uric acid levels caused by purine ingestion and accelerated urinary uric acid excretion in subjects with lower urate excretion using a randomized, single-blind, placebo-controlled, crossover clinical trial design. Healthy Japanese adult males with lower urate excretion ingested water containing purines in addition to dextrin (place

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Li Kam Wa, T. C., S. Freestone, R. R. Samson, N. R. Johnson, and M. R. Lee. "A Comparison of the Renal and Neuroendocrine Effects of Two 5-Hydroxytryptamine Renal Prodrugs in Normal Man." Clinical Science 85, no. 5 (1993): 607–14. http://dx.doi.org/10.1042/cs0850607.

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1. The effects of 1 h intravenous infusions of equimolar amounts (45 nmol min−1 kg−1) of two putative 5-hydroxytryptamine renal prodrugs, 5-hydroxy-L-tryptophan and γ-L-glutamyl-5-hydroxy-L-tryptophan, were investigated in a randomized, placebo-controlled, cross-over study in nine healthy male subjects. 2. Cumulative urinary 5-hydroxytryptamine excretion over the 3 h observation period rose by about 370-fold after 5-hydroxy-L-tryptophan and 390-fold after γ-L-glutamyl-5-hydroxy-L-tryptophan when compared with placebo infusion. Urinary 5-hydroxy-L-tryptophan excretion was three times higher aft

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3

Egashira, Yukari, Shin Nagaki, and Hiroo Sanada. "Tryptophan-Niacin Metabolism in Rat with Puromycin Aminonucleoside-Induced Nephrosis." International Journal for Vitamin and Nutrition Research 76, no. 1 (2006): 28–33. http://dx.doi.org/10.1024/0300-9831.76.1.28.

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We investigated the change of tryptophan-niacin metabolism in rats with puromycin aminonucleoside PAN-induced nephrosis, the mechanisms responsible for their change of urinary excretion of nicotinamide and its metabolites, and the role of the kidney in tryptophan-niacin conversion. PAN-treated rats were intraperitoneally injected once with a 1.0% (w/v) solution of PAN at a dose of 100 mg/kg body weight. The collection of 24-hour urine was conducted 8 days after PAN injection. Daily urinary excretion of nicotinamide and its metabolites, liver and blood NAD, and key enzyme activities of tryptoph

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Valko-Rokytovská, Marcela, Beáta Hubková, Anna Birková, et al. "Specific Urinary Metabolites in Malignant Melanoma." Medicina 55, no. 5 (2019): 145. http://dx.doi.org/10.3390/medicina55050145.

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Background and objectives: Melanin, which has a confirmed role in melanoma cell behaviour, is formed in the process of melanogenesis and is synthesized from tryptophan, L-tyrosine and their metabolites. All these metabolites are easily detectable by chromatography in urine. Materials and Methods: Urine samples of 133 individuals (82 malignant melanoma patients and 51 healthy controls) were analysed by reversed-phase high-performance liquid chromatography (RP-HPLC). The diagnosis of malignant melanoma was confirmed histologically. Results: Chromatograms of melanoma patients showed increased lev

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Wa, T. C. Li Kam, S. Freestone, R. R. Samson, N. R. Johnston, and M. R. Lee. "Renal Metabolism and Effects of the Glutamyl Derivatives of l-Dopa and 5-Hydroxytryptophan in Man." Clinical Science 91, no. 2 (1996): 177–85. http://dx.doi.org/10.1042/cs0910177.

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1. Equimolar amounts of y-l-glutamyl-l-3,4-dihydroxyphenylalanine (gludopa) and γ-l-glutamyl-5-hydroxy-l-tryptophan were infused separately and together in eight healthy, salt-replete male subjects in a placebo-controlled, cross-over study to investigate whether the administration of one amine precursor affects the renal metabolism of the other and to determine whether dopamine or 5-hydroxytryptamine would be generated preferentially. The overall effect on sodium excretion was also measured when both precursors were administered simultaneously. 2. Administration of gludopa was associated with

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6

Post, Adrian, Marleen Huberts, Enya Poppe, et al. "Tryptophan Intake and Tryptophan Losses in Hemodialysis Patients: A Balance Study." Nutrients 11, no. 12 (2019): 2851. http://dx.doi.org/10.3390/nu11122851.

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Tryptophan depletion is common in hemodialysis patients. The cause of this depletion remains largely unknown, but reduced nutritional tryptophan intake, losses during dialysis or an increased catabolism due to an inflammatory state are likely contributors. Currently, little is known about tryptophan homeostasis in hemodialysis patients. We assessed dietary tryptophan intake, measured plasma tryptophan during dialysis, and measured the combined urinary and dialysate excretion of tryptophan in 40 hemodialysis patients (66 ± 15 years and 68% male). Patients had low tryptophan concentrations (27 ±

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7

Williams, David J. "Tryptophan, urinary quinolines, and bladder cancer." Nutrition and Cancer 11, no. 2 (1988): 81–82. http://dx.doi.org/10.1080/01635588809513973.

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8

Fregly, Melvin J., Colin Sumners, and J. Robert Cade. "Effect of chronic dietary treatment with L-tryptophan on the maintenance of hypertension in spontaneously hypertensive rats." Canadian Journal of Physiology and Pharmacology 67, no. 6 (1989): 656–62. http://dx.doi.org/10.1139/y89-105.

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Chronic dietary administration of L-tryptophan at 2.5 and 5.0% by weight reduced the elevated systolic blood pressure of spontaneously hypertensive (SH) rats. Blood pressure was reduced significantly by 3 weeks after initiation of treatment and continued to fall during the course of the 15 weeks of treatment. Body weights of the treated rats were not affected significantly by treatment, nor were daily food and fluid intakes and urine outputs. SH rats, treated with the higher dose of tryptophan, also significantly reduced their urinary outputs of epinephrine and norepinephrine compared with SH

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9

Engin, Ayse Basak, Bensu Karahalil, Ali Esat Karakaya, and Atilla Engin. "Exposure to Helicobacter pylori and Serum Kynurenine to Tryptophan Ratio in Patients with Gastric Cancer." Pteridines 21, no. 1 (2010): 110–20. http://dx.doi.org/10.1515/pteridines.2010.21.1.110.

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Abstract In Helicobacter pylori seropositive individuals, the subsequent risk of non-cardia gastric cancer development is frequently attributed to the infection agent. Although the link between inflammation and gastric cancer is formally recognized, the molecular basis of evading mechanisms of Helicobacter pylori from host immune system remains unclear. The aim of this study was to determine the effect of systemic factors in gastric cancer patients such as serum kynurenine to tryptophan ratios, neopterin, nitric oxide and urinary biopterin levels which may sustain the persistence of Helicobact

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Fukuwatari and Shibata. "Effect of Nicotinamide Administration on the Tryptophan-Nicotinamide Pathway in Humans." International Journal for Vitamin and Nutrition Research 77, no. 4 (2007): 255–62. http://dx.doi.org/10.1024/0300-9831.77.4.255.

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The vitamin nicotinamide is synthesized in the liver from tryptophan, and distributed to non-hepatic tissues. Although it is generally accepted that 60 mg tryptophan is equivalent to 1 mg nicotinamide in humans, the conversion ratio of tryptophan to nicotinamide is changeable. To determine if de novo nicotinamide synthesis from tryptophan is influenced by nicotinamide intake itself, six young women consumed controlled diets containing 30.4 or 24.8 mg niacin-equivalent nicotinamide supplements with 0, 89, 310, or 562 μmol/day (0, 10.9, 37.8, or 68.6 mg/day, respectively), and urinary excretion

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Book chapters on the topic "Urinary tryptophan"

1

Yuyama, S., and T. Suzuki. "URINARY EXCRETION OF TRIGONELLINE AND N1-METHYL NICOTINAMIDE BY HUMAN BEINGS AND RATS FOLLOWING ORAL ADMINISTRATION OF NICOTINIC ACID OR TRIGONELLINE." In Progress in Tryptophan and Serotonin Research 1986, edited by David A. Bender, Michael H. Joseph, Walter Kochen, and Hans Steinhart. De Gruyter, 1987. http://dx.doi.org/10.1515/9783110854657-052.

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Milovanović, D. D., Lj Milovanović, and D. Vranješević’. "Serum Tryptophan to Large Neutral Amino Acid Ratio and Urinary Tryptophan in Three Patients with Phenylketonuria in a Family." In Advances in Experimental Medicine and Biology. Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4709-9_37.

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Milovanovic, Dragoslav D. "A Clinicobiochemical Study of Tryptophan and Other Plasma and Urinary Amino Acids in the Family With Hartnup Disease." In Advances in Experimental Medicine and Biology. Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0135-0_36.

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Knoers, Nine V. A. M., and Elena N. Levtchenko. "Disorders of tubular electrolyte handling." In Oxford Textbook of Medicine, edited by John D. Firth. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0506.

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Glycosuria—glucose reabsorption in the proximal tubule is carried out by two different pairs of apical Na<sup>+</sup>-dependent (SGLT1 and -2) and basolateral Na<sup>+</sup>-independent (GLUT1 and -2) glucose transporters. Abnormalities in renal glucose transport can be seen in association with other defects of proximal tubular transport. Familial renal glycosuria is a rare autosomal recessive condition caused by mutations in the SGLT2-encoding gene, SLC5A2. Phosphate-handling disorders—the plasma concentration of inorganic phosphate depends on the balance between intestinal absorption, renal

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Middleton, Stephen J., and Raymond J. Playford. "Bacterial overgrowth of the small intestine." In Oxford Textbook of Medicine, edited by Jack Satsangi. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0299.

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Small intestinal bacterial overgrowth can be defined as the presence of excessive bacteria in the small intestine which can interfere with digestion and absorption. Predisposing causes include sustained hypochlorhydria induced by proton pump inhibitors, small intestinal dysmotility and stasis due to anatomical or motor abnormalities, and reduced antibacterial activity as seen in immunological deficiency and chronic pancreatitis. Presentation is predominantly from consequences of malabsorption, including gastrointestinal symptoms (e.g. diarrhoea or steatorrhoea) and features of specific nutrien

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