A fluorimetric and enzymatic method for the estimation of serum total bile acids

Murphy, Gérard M.; Billing, Barbara H.; Baron, D N

doi:10.1136/jcp.23.7.594

Cited by 233 publications

(85 citation statements)

References 13 publications

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“…Serum bile acid levels were not affected by sex (Schwarz et al 1974; Shaffer and Gordon 1978; Barbara et al 1980;Starkey and Marks 1982), whereas the levels are slightly high in females (Murphy et al 1970) or in males (Mashige et al 1976). The results of the present study indicated that no sex-related differences could be observed statistically for any of serum bile acids in all age groups, suggesting that age and sex insignificantly affect bile acid metabolic profiles in healthy adults as far as serum bile acids are concerned and serum bile acid determinations are clinically useful as a liver function test in a wide range of age.…”

Section: Discussionmentioning

confidence: 95%

“…Earlier studies have partially included healthy subjects as old as those in our study (Murphy et al 1970;Schwarz et al 1974;Mashige et al 1976 ;Shaffer and Gordon 1978;Starkey and Marks 1982). When the correlation of age to serum bile acid levels in a large proportion of healthy adults was studied by the enzymatic fluorometric method, no age-related differences were observed for PBA, TBA and P/T ratio which reflects the conditions of intestinal microflora and serum bile acid levels in adults were maintained at nearly normal levels even at very advanced age.…”

Section: Discussionmentioning

confidence: 97%

See 1 more Smart Citation

Age- and sex-related profiles of serum primary and total bile acids in infants, children and adults.

Kawasaki

Yamanishi²,

Miyake

et al. 1986

Tohoku J. Exp. Med.

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The relation of age and sex to serum primary (PBA) and total bile acid (TBA) concentrations was evaluated by an enzymatic fluorometric microassay in healthy infants, children and adults. TBA concentrations were the highest in the 6-dayold group and 1-month-old group and seemed to switch to almost normal adult levels by the age of 4-6 years, which persisted throughout life, while PBA concentrations were predominant over a period of 3 days to 3 months after birth. No sex-related differences were observed from neonates to very old persons for any of serum bile acids. These results show that the bile acid metabolism in the liver and the enterohepatic circulation of bile acids are usually matured in infancy and that aging and sex may insignificantly affect serum bile acid metabolic profiles.age ; sex ; primary bile acids ; total bile acids

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 97%

Age- and sex-related profiles of serum primary and total bile acids in infants, children and adults.

Kawasaki

Yamanishi²,

Miyake

et al. 1986

Tohoku J. Exp. Med.

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“…Bile salt concentration was determined by the 3␣-hydroxysterol dehydrogenase method. 35 Cholesterol and phospholipids were measured after lipid extraction 36 according to the methods of Gamble et al 37 and Bötcher et al, 38 respectively.…”

Section: Methodsmentioning

confidence: 99%

Effective oral treatment of unconjugated hyperbilirubinemia in Gunn rats

et al. 2005

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We sought to develop an oral treatment for unconjugated hyperbilirubinemia. In the Gunn rat model of unconjugated hyperbilirubinemia, dietary supplementation with the lipase inhibitor orlistat (Orl) or with calcium phosphate (CaP) decreases plasma unconjugated bilirubin (UCB) levels. We determined whether Orl, CaP, or their combination is superior to phototherapy, the conventional treatment, and whether the effects of Orl and CaP are influenced by dietary fat content. Gunn rats were treated with Orl (200 mg/kg chow), CaP (20 g/kg chow), Orl ؉ CaP, or continuous phototherapy (19 W/cm 2 /nm) during a low-fat (LF) diet (13 energy%) or high-fat (HF) diet (35 energy%). Plasma UCB and fecal fat excretion were measured before, during, and/or at the end of treatment. Orl treatment for 2 weeks (HF diet) reduced plasma UCB concentrations similar to phototherapy (؊34% and ؊28%, respectively); the combination of both was more effective than either treatment alone (؊48%; P < .001). After 3 weeks of a HF diet, plasma UCB was 46% lower compared with the LF diet (P < .001). Plasma UCB concentrations were negatively correlated with fecal fat excretion (r ‫؍‬ ؊0.96; P < .001). Irrespective of dietary fat content, 3 weeks of combined treatment (Orl ؉ CaP) decreased plasma UCB by approximately 50% (P < .01) and was more effective than phototherapy (P < .05) at the intensity provided. C rigler-Najjar disease is characterized by a permanent unconjugated hyperbilirubinemia due to absent (type I) or decreased (type II) activity of the hepatic enzyme bilirubin-UDP-glucuronosyltransferase. 1 Severe unconjugated hyperbilirubinemia can lead to bilirubin encephalopathy, kernicterus, and death. 2,3 Phenobarbital treatment can usually control unconjugated hyperbilirubinemia in Crigler-Najjar type II patients via residual enzyme induction. 4,5 Phenobarbital is not effective in Crigler-Najjar disease type I, however, so these patients have to undergo daily phototherapy, which has considerable disadvantages. Phototherapy becomes less effective with age, probably due to skin alterations, 6,7 a decrease in the surface area to body mass ratio, 8 and a diminishing compliance to the intensive phototherapy regimen, which may take up to 12 hours per day. 6 To prevent irreversible brain damage due to kernicterus, many patients with CriglerNajjar disease type I undergo liver transplantation in their second decade. 9,10 We sought to develop an alternative treatment for unconjugated hyperbilirubinemia based on oral administration and with equal or higher efficacy than phototherapy. The oral treatment strategy used in the present study is based on reducing the reabsorption of UCB 11,12 through intestinal capture. Reabsorption of UCB can contribute substantially to the pathogenesis

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“…Bile salts were measured enzymatically. 21 Commercially available kits were used for the determination of unesterified and total cholesterol, triglycerides (Roche, Mannheim, Germany), phospholipids and free fatty acids (Wako, Neuss, Germany) in plasma. Hepatic and biliary lipids were extracted following Bligh and Dyer.…”

Section: Methodsmentioning

confidence: 99%

MdrP-glycoproteins are not essential for biliary excretion of the hydrophobic heme precursor protoporphyrin in a griseofulvin-induced mouse model of erythropoietic protoporphyria

et al. 2002

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Hepatic complications in erythropoietic protoporphyria (EPP) have been attributed to toxic actions of accumulated protoporphyrin (PP). PP can only be removed via the bile but transport systems involved have not been defined. The aim of this study was to gain insight in the mode of biliary PP excretion, with emphasis on the potential contribution of the Mdr1 P-glycoprotein export pump and biliary lipids as PP carriers. Control mice and mice homozygous for Mdr1a/b (Abcb1) or Mdr2 (Abcb4) gene disruption, the latter unable to secrete phospholipids and cholesterol into bile, were treated with griseofulvin to chemically induce protoporphyria. All groups showed dramatically increased PP levels in erythrocytes and liver after griseofulvin treatment. Histologically, massive PP deposits were found in livers of control and Mdr1a/b ؊/؊ mice but not in those of Mdr2 ؊/؊ mice. Serum unesterified cholesterol and phospholipids were increased by griseofulvin because of formation of lipoprotein-X in control and Mdr1a/b ؊/؊ mice only. Yet, bile flow was not impaired in griseofulvintreated mice, and biliary bile salt, phospholipid, and cholesterol secretion rates were significantly increased. Surprisingly, biliary PP excretion was similar in all 3 groups of griseofulvin-treated mice: the observed linear relationship between hepatic and biliary PP concentrations and identical liver-to-bile concentration ratios in treated and untreated mice suggest a passive mode of excretion. In conclusion, the data show that Mdr P-glycoproteins are not critically involved in biliary removal of excess PP and indicate that the presence of biliary lipids is required for formation of intrahepatic PP deposits. (HEPATOLOGY 2002;35: 299-306.) F errochelatase (EC 4.99.1.1) is a mitochondrial enzyme that transfers iron into protoporphyrin (PP) during the formation of heme. 1 In erythropoietic protoporphyria (EPP), an inherited disease caused by a mutated ferrochelatase gene, ferrochelatase activity is markedly reduced, i.e., in severe cases to 4% to 20% of control values. 2 Impaired ferrochelatase activity leads to a reduced heme synthesis rate and, via induction of the preceding steps in the biosynthetic cascade, to accumulation of the highly hydrophobic heme precursor PP in erythrocytes and liver. 1 Common clinical signs of EPP are erythema and edema caused by PP phototoxicity in the skin. 3 In the liver, PP deposits can be found both in cells and in small bile channels. 4 Severe hepatic complications in EPP are relatively rare, but indicative for transplantation in up to 10% of all cases. 5 PP is not enzymatically altered nor conjugated in the liver. 4 It is highly hydrophobic and is therefore removed from the body exclusively via the bile, followed by fecal excretion. 6 Mechanisms responsible for PP secretion into bile are currently not known. Previous studies performed by our laboratory showed association of PP with cholesterol/phospholipid vesicles in bile, 7 suggesting that these may act as PP carriers in this aqueous solution. Reduction of bilia...

show abstract

A fluorimetric and enzymatic method for the estimation of serum total bile acids

Cited by 233 publications

References 13 publications

Age- and sex-related profiles of serum primary and total bile acids in infants, children and adults.

Age- and sex-related profiles of serum primary and total bile acids in infants, children and adults.

Effective oral treatment of unconjugated hyperbilirubinemia in Gunn rats

MdrP-glycoproteins are not essential for biliary excretion of the hydrophobic heme precursor protoporphyrin in a griseofulvin-induced mouse model of erythropoietic protoporphyria

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