Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Urine bile acids

Goto T, Shibata A, Sasaki D, Suzuki N, Hishinuma T, Kakiyama G, Iida T, Mano N, Goto J (2005) Identification of a novel conjugate in human urine bile acid acyl galactosides. Steroids 70 185-192... [Pg.663]

Endogenous and exogenous androgens can be derivatized with trimethylsilyl (TMS) for hydroxy functions and by 0-methylation for ketones, and analyzed with GC-FID or GC-MS (Shimada et al., 2001). MS is more prevalent due to unequivocal identification and greatly increased sensitivity but FID is still used in laboratories for some steroids. Sterols have typically been analyzed by GC-FID and GC-MS with derivatization to optimize peak shape (Shimada et al., 2001), and bile acids can be derivatized with M-butyl ester-TMS ether and analyzed by GC-FID from plasma samples (Batta et al., 1998). Juricskay and Telegdy (2000) reported an assay capable of analyzing 28 steroids in urine samples using GC-FID. [Pg.9]

In vivo, measuring bile acids in plasma and urine should be revived as potential biomarkers in the modern metabolomic era. Then the first-order scientific question will become whether early and time-controlled fasting-level measurement of bile acid concentration in plasma and urine can become a sensitive and specific biomarker for drug-induced cholestasis and ultimately liver injury at later time-points [117] Clinical trials should be conducted to evaluate whether such bile acid measurements can be used as part of a predictive panel to identify patients who are at increased risk of drug-induced cholestasis. [Pg.368]

Peroxisomal disorders (Zellweger syndrome, Refsum s disease, neonatal adre-noleukodystrophy) are characterised by defective peroxisome biogenesis, or, being present, peroxisomes lacking / -oxidative enzymes. In the BA biosynthetic pathway, dihydroxycoprostanic acid (DHCA) and trihydroxycoprostanic acid (THCA) are /1-oxidised in peroxisomes to produce CA and CDCA, respectively, whereas peroxisomal disorders cause a defective oxidation of the BA precursor side chain, which leads to an accumulation of C27 bile acids, notably 3 ,7 -dihydroxy-5/3-cholesta-noic acid (DHCA) and 3a,7a,12a-trihydroxy-5/l-cholestanoic acid (THCA), in the plasma and urine of affected patients. [Pg.611]

Alme B, Bremmelgaard A, Siovall J, Thomassen P (1977) Analysis of metabolic profiles of bile acids in urine using a lipophilic anion exchanger and computerized gas-liquid chromatography-mass spectrometry. J Lipid Res 18 339-362... [Pg.664]

Although bile acid conjugates with amino acids are normally excreted into bile, amino acid conjugates of xenobiotics are usually excreted into urine. Conjugation with endogenous amino acids facilitates urinary excretion because of the organic anion transport systems located in the kidney tubules. [Pg.114]

Taurine conjugation with bile acids, phenylacetic acid, and indolylacetic acid seems to be a minor process in most species, but in the pigeon and ferret, it occurs extensively. Other infrequently reported conjugations include serine conjugation of xanthurenic acid in rats excretion of quinaldic acid as quinaldylglycyltaurine and quinaldylglycylglycine in the urine of the cat, but not of the rat or rabbit and conversion of furfural to furylacrylie acid in the dog and rabbit, but not in the rat, hen, or human. The dog and... [Pg.178]

Plasma and urine samples from atherosclerotic and control rats were comparatively analyzed by ultrafast liquid chromatography coupled with ion trap-time-of-flight (IT-TOF) MS (UFLC-IT/TOF-MS) (16). They identified 12 metabolites in rat plasma and 8 metabolites in rat urine as potential biomarkers. Concentrations of leucine, phenylalanine, tryptophan, acetylcar-nitine, butyrylcamitine, propionylcamitine, and spermine in plasma and 3-0-methyl-dopa, ethyl /V2-acety I -1. -argininate, leucylproline, glucuronate, A(6)-(A-threonylcarbonyl)-adenosine, and methyl-hippuric acid in urine were decreased in atherosclerosis rats ursodeoxycholic acid, chenodeoxycholic acid, LPC (06 0), LPC (08 0), and LPC (08 1) in plasma and hippuric acid in urine were increased in atherosclerosis rats. The altered metabolites demonstrated abnormal metabolism of phenylalanine, tryptophan, bile acids, and amino acids. Lysophosphatidylcholine (LPC) plays an important role in inflammation and cell proliferation, which shows a relationship between LPC in the progress of atherosclerosis and other inflammatory diseases. [Pg.290]

Slightly hindered hydroxyl groups of bile acids can be silylated according to the procedure of Makita and Wells [319] methyl esters of bile acids, prepared by treatment with diazomethane, are dissolved in anhydrous pyridine (ca. 1 ml per 10 mg) and 0.1 ml of HMDS and 0.03 ml of TMCS are added to this solution. After standing for 10 min at room temperature an aliquot of the reaction mixture is injected directly. The method was applied to the determination of faecal bile acids in the rat. Other workers [320] investigated the retention behaviour of 52 persilylated methyl esters of urine acids on QF-1, OV-1 and OV-17 stationary phases. They correlated the data expressed as relative retention times with the structures of the compounds. [Pg.153]

The derivatives were said to be more stable than TMS ethers so that losses in the column were avoided. The ECD response did not differ much from that of the FID and hence the significance of these derivatives is mainly that they can be better separated from interfering components and used for identification. The derivatives have been used for the analysis of methyl esters of bile acids [334] and androstane in urine [335], They also proved useful in combination with mass spectrometry [336,337] as they provided characteristic mass spectra. [Pg.155]

The usefulness of low-energy MS/MS has been shown in the diagnosis of metabolic diseases by analysis of underivatized bile acids, conjugated or not, in complex biological samples such as urine or serum. A series of neutral loss and precursor ion scans was... [Pg.384]

A) The FAB spectrum of a mixture of 11 bile acids from a patient s urine, measured in negative mode. (B) Spectrum of the 124 Th precursors, allowing the selective detection of taurine conjugates. (C) Spectrum of 62 Da neutral losses. (D) Spectrum of 152 Da neutral losses. Reproduced (modified) from Libert R., Hermans D., Draye J.R, Van Hoof F., Sokal E., and de Hoffmann E., Clin. Chem., 37, 2102-2110, 111. [Pg.385]

From 1966 to 1986 Horning was Director of the Institute of Lipid Research, Chairman of the Biochemistry Department (1962-1966), and Professor of Chemistry at Baylor College of Medicine (1961-1986). During this period he applied gas chromatography to steroids in human fluids, urine, bile and spinal liquids, and to amino add derivatives. His group isolated acids, alcohols, and waxes from human skin. Here they applied mass spectrometry and liquid or gas chromatography to the identification of numerous human substances. They extended these techniques to investigations of the metabolism of many different compounds in humans. [Pg.302]

The existence of bile-acid glucosiduronates in urine and plasma of man under certain pathological conditions has now been recognized197,198 for identification purposes, several bile acid-3-yl /3-d-glucopyranosiduronic acids have been synthesized199 by the Koenigs-Knorr method. [Pg.95]

Unlike the other fat-soluble vitamins, there is litde or no storage of vitamin D in the liver, except in oily fish. In human liver, concentrations of vitamin D do not exceed about 25 nmol per kg. Significant amounts may be present in adipose tissue, but this is not really storage of the vitamin, because it is released into the circulation as adipose tissue is catabolized, rather than in response to demand for the vitamin. The main storage of the vitamin seems to be as plasma calcidiol, which has a half-life of the order of 3 weeks (Holick, 1990). In temperate climates, there is a considerable seasonal variation, with plasma concentrations at the end of winter as low as half those seen at the end of summer (see Table 3.2). The major route of vitamin D excretion is in the bile, with less than 5% as a variety of water-soluble conjugates in urine. Calcitroic acid (see Figure 3.3) is the major product of calcitriol metabolism but, in addition, there are a number of other hydroxylated and oxidized metabolites. [Pg.80]

Bile acid production amounts to 400-500 mg/day (ca. 1 mmol). Excretion in the stool is of a similar order accordingly, renewed synthesis of bile acids is determined by the daily loss. Excretion in the urine lies below 0.5 mg/day (8 gmol/day) - this small amount may be disregarded. [Pg.36]

The sensitivity of values determined 2 hours after food consumption seems to be higher than that after fasting. The fasting value is, however, preferred for the sake of reproducibility. In liver diseases, the postprandial increase in serum values can be several times higher than after fasting. In healthy individuals, however, fasting values are only exceeded by 50-70%. The elevation of bile acids in the serum is reflected by an increase in their excretion in the urine (normal < 8 gmol/day). The elevated level of bile acids returns to normal at a relatively slow pace. [Pg.101]

Enzymatic activity 2. Synthesis capacity 3. Excretion capacity GPT, y-GT — ChE, — Quick s value AP, bile pigments — in the urine GOT, GDH — albumin — bilirubin, LAP — LDH ammonia, galactose EC bile acids, iron, copper, cholesterol, indocyanine green, LPX... [Pg.122]

Determination of total bilirubin with differentiation between direct (conjugated) and indirect (unconjugated) bilirubin Determination of cholestasis-indicating enzymes (AP, LAP, y-GT) bile acids and bile pigments in the urine (s. tab. 12.6) Test for signs of haemolysis (s. tab. 12.3)... [Pg.224]

In each form of cholestasis, atypical bile adds, such as monohydroxy bile acids, aUo-bile adds, 1- or 6-hydroxylated bile acids and their sulphated or glucuronidated derivatives, are found in the sermn and/or urine. In cholestasis, the increase in the neosynthesis of atypical bile adds that pass into the kidney can be seen as a compensatory mechanism which eliminates potentially hepatotoxic bile acids by renal clearance. The highest renal excretion quota is demonstrated by tetrahydroxy bile acids. [Pg.236]

In summary, these studies demonstrated that in CTX the impaired synthesis of bile acids is due to a defect in the biosynthetic pathway involving the oxidation of the cholesterol side-chain. As a consequence of the inefficient side-chain oxidation, increased 23, 24 and 25-hydroxylation of bile acid precursors occurs with the consequent marked increase in bile alcohol glucuronides secretions in bile, urine, plasma and feces (free bile alcohols). These compounds were isolated, synthesized and fully characterized by various spectroscopic methods. In addition, their absolute stereochemistiy determined by Lanthanide-Induced Circular Dichroism (CD) and Sharpless Asymmetric Dihydroxylation studies. Further studies demonstrated that (CTX) patients transform cholesterol into bile acids predominantly via the 25-hydroxylation pathway. This pathway involves the 25-hydroxylation of 5P-cholestane-3a,7a, 12a-triol to give 5P-cholestane-5P-cholestane-3a,7a,12a,25- tetrol followed by stereospecific 24S-hydroxylation to yield 5P-cholestane-3a,7a,12a,24S,25-pentol which in turn was converted to cholic acid. [Pg.222]


See other pages where Urine bile acids is mentioned: [Pg.659]    [Pg.194]    [Pg.197]    [Pg.143]    [Pg.32]    [Pg.66]    [Pg.291]    [Pg.43]    [Pg.15]    [Pg.231]    [Pg.222]    [Pg.291]    [Pg.346]    [Pg.270]    [Pg.118]    [Pg.216]    [Pg.150]    [Pg.104]    [Pg.731]    [Pg.334]    [Pg.194]    [Pg.194]    [Pg.955]    [Pg.80]    [Pg.156]    [Pg.34]    [Pg.647]    [Pg.648]    [Pg.207]    [Pg.216]   
See also in sourсe #XX -- [ Pg.258 , Pg.291 , Pg.292 , Pg.321 , Pg.322 , Pg.323 ]




SEARCH



Acids urine

Urine bile acid conjugates found

© 2024 chempedia.info