Enzymatic determination of cholesterol in bile

Roda, Aldo; Festi, Davide; Sama, C; Mazzella, Giuseppe; Aldini, Rita; Roda, Enrico; Barbara, L

doi:10.1016/0009-8981(75)90364-2

Cited by 156 publications

(44 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[15][16][17] The qualitative and quantitative composition of the bile, in terms of the individual BA, was determined by different combined chromatographic techniques. Bile sample underwent preliminary clean-up using conventional C-18 reverse-phase extraction (C-18 Bond Elut, Analytichem International, Harbor City, CA), which allows a complete recovery of all the studied BA as previously reported.…”

Section: Methodsmentioning

confidence: 99%

Taurohyodeoxycholic acid protects against taurochenodeoxycholic acid-induced cholestasis in the rat

et al. 1998

View full text Add to dashboard Cite

The prevention of the hepatotoxic effects produced by intravenous infusion of taurochenodeoxycholic acid (TCDCA) by coinfusion with taurohyodeoxycholic acid (THDCA) was evaluated in bile fistula rats; the hepatoprotective effects of the latter were also compared with those of tauroursodeoxycholic acid (TUDCA). Rats infused with TCDCA at a dose of 8 mol/min/kg showed reduced bile flow and calcium secretion, as well as increased biliary release of alkaline phosphatase (AP) and lactate dehydrogenase (LDH). This was associated with a very low biliary secretion rate of TCDCA (Ϸ1 mol/min/kg). Simultaneous infusion of THDCA or TUDCA at the same dose preserved bile flow and almost totally abolished the pathological leakage of the two enzymes into bile. The effect was slightly more potent for THDCA. The maximum secretion rate of TCDCA increased to the highest value (8 mol/min/kg) when coinfused with either of the two hepatoprotective bile acids (BA), which were efficiently and completely secreted in the bile, without metabolism. Calcium output was also restored and phospholipid (PL) secretion increased with respect to the control saline infusion. This increase was higher in the THDCA study. These data show that THDCA is highly effective in the prevention of hepatotoxicity induced by intravenous infusion of TCDCA by facilitating its biliary secretion and reducing its hepatic residence time; this was associated with selective stimulation of PL biliary secretion. (HEPATOLOGY 1998;27:520-525.)Taurohyodeoxycholic acid (THDCA) is the taurineamidated form of hyodeoxycholic acid, a natural bile acid present in the pig, other animal species, and also in humans. [1][2][3][4] The steroid structure is characterized by the presence of two hydroxy groups, 3␣ and 6␣, the latter of which is equatorial and oriented toward the back of the steroid moiety. As a result, this molecule is less detergent than the other dihydroxy bile acid (BA), such as chenodeoxycholic acid (CDCA) (3␣, 7␣) or its 3␣, 6␤ dihydroxy epimer. The hydrophobic-hydrophilic balance of THDCA resembles that of tauroursodeoxycholic acid (TUDCA), with which it also shares similar orientation of the 7␤ hydroxy group with respect to the 6␣ hydroxyl. The physicochemical properties of this molecule are quite similar to those of TUDCA in terms of lipophilicity and critical micellar concentration (CMC). 5,6 Because of its relatively high hydrophilicity, THDCA has been proposed for use as an alternative to ursodeoxycholic acid (UDCA) or TUDCA for the treatment of cholesterol gallstone dissolution. [7][8][9][10] Recent studies have reported its activity as a cholesterol-dissolving agent, both in vitro and in vivo, and this has been attributed to its ability to selectively stimulate biliary phospholipid secretion. 11 Moreover, hyodeoxycholic acid is a secondary BA derived from hyocholic acid by intestinal bacterial 7␣ dehydroxylation, and thus, it is quite stable to intestinal bacteria; this is a potential advantage compared with UDCA that can undergo either 7␤ dehydroxylation or 7␣...

show abstract

Section: Methodsmentioning

confidence: 99%

Taurohyodeoxycholic acid protects against taurochenodeoxycholic acid-induced cholestasis in the rat

et al. 1998

View full text Add to dashboard Cite

show abstract

“…Blood was taken at 2,4,6,8,10,12,16,19,22,25,30,40,50,70,90,135 and 180 min for immediate determination of glucose and later for plasma insulin measurements. In addition, three baseline samples were taken 15, 10 and 5 min before the glucose injection.…”

Section: Insulin Sensitivitymentioning

confidence: 99%

“…The concentration of cholesterol was determined with the Cholesterol Kit (BoeringeraMannheim, Mannheim, Germany) at 405 nm on a spectrophotometer (Beckman 25, Beckman Instruments, Fullerton, CA, USA). 30 The concentration of bile acid was determined with an enzymatic kit (Sterognost 3-alfa-Pho, Nycomed DAK, Copenhagen, Denmark). The bile was diluted with sterile NaCl 1 : 6 and centrifuged at 3000 g/min for 10 min and bile acid content was determined by spectrophotometer (Shimadzu UV160A, Kyoto, Japan) at 340 nm.…”

Section: Lithogenic Indexmentioning

confidence: 99%

“…After fasting overnight, the subjects ingested a standardised meal containing 37.5 g fat, 30.0 g protein and 38.7 g carbohydrate (Danish open sandwiches and milk). Five minutes before the meal and 5, 10, 20, 30, 40, 50, 60, 120 and 150 min postprandially, blood was collected in ice-chilled tubes containing 3.9 mmol of EDTA (ethylenediaminetetra-acetate) per ml of blood.…”

Section: Meal Stimulated Cck Releasementioning

confidence: 99%

See 1 more Smart Citation

Fasting gall bladder volume and lithogenicity in relation to glucose tolerance, total and intra-abdominal fat masses in obese non-diabetic subjects

et al. 1998

View full text Add to dashboard Cite

OBJECTIVE: To investigate whether total body fat mass or fat distribution and associated metabolic disturbances in glucose and lipid metabolism in¯uence the well known gallstone pathogenetic factors in obese subjects in order to explain why some obese subjects develop gallstones and some do not. DESIGN: Cross sectional study of gallstone pathogenetic factors, body composition, fat distribution, glucose and lipid metabolism. SUBJECTS: 57 healthy overweight subjects (aged 26±64 y, body mass index (BMI) 30±45 kg/m 2 ). MEASUREMENTS: Total and intra-abdominal fat masses were measured by dual X-ray absorptiometry and abdominal CT scanning, respectively. The lithogenic index was measured in aspirated bile. The gallbladder volume was determined by ultrasound and the gallbladder ejection fraction% by dynamic cholescintigraphy. Plasma cholecystokinin (CCK) concentrations during a meal were measured with a speci®c radioimmunoassay. Insulin sensitivity was measured by the Minimal Model and glucose tolerance by an oral glucose tolerance test (OGTT). Serum lipid concentrations were measured by standard methods. RESULTS: The gallbladder volume in the fasting state increased with increasing intra-abdominal fat mass (P 0.006) and was increased in subjects with impaired glucose tolerance (41 vs 27 ml, P 0.001). The lithogenic index was b 1 in all subjects and correlated with total fat mass (P 0.04). CONCLUSION: Gallstone pathogenesis in obesity seems to be in¯uenced by the total body fat mass and its regional distribution possibly via mutual association with the glucose tolerance.

show abstract

“…Total bile acid concentration was measured by the 3 a-hydroxysteroid dehydrogenase enzyme assay as described by Talalay (1960) and modified by Admirand & Small (1968). Phospholipids were measured by the method of Bartlett (1959) and cholesterol was measured by the cholesterol oxidase method in an aliquot that was diluted at the bedside in isopropanol (1 in 10; Roda et al, 1975). Saturation index (SI) was calculated using the polynomial equation developed by Thomas & Hofmann (1973), based on the limits of cholesterol solubility described by Hegardt & Dam (1971) and Holzbach et al (1973).…”

Section: Methodsmentioning

confidence: 99%

Effect of sodium acetyl salicylate on cholesterol saturation of fasting gall bladder bile, with and without chenic acid.

Kupfer¹,

Northfield²

1983

Brit J Clinical Pharma

View full text Add to dashboard Cite

The aims of this study were (a) to determine whether sodium acetyl salicylate by itself or in combination with chenodeoxycholic (chenic) acid would decrease the cholesterol saturation index (SI) of fasting gall bladder bile in man; and (b) to confirm prospectively that 8 mg kg-' day-chenic acid given at bedtime together with a low cholesterol diet reduces gall bladder bile SI to a level where consistent gallstone dissolution would be expected.Seven patients were studied on each of the following regimens given in random order for 1 month each: bedtime chenic acid alone 8 mg kg-'day-'; sodium acetyl salicylate alone 600 mg four times daily; bedtime chenic acid together with sodium acetyl salicylate; no treatment. Gall bladder samples were taken by nasoduodenal intubation at the end of each regimen and SI determined.SI (mean + s.e. mean) on low cholesterol diet with no drug treatment was 1.14 + 0.06. On bedtime chenic acid 8 mg kg-' day-' plus low cholesterol diet it fell to 0.83 + 0.03 (P < 0.05). Sodium acetyl salicylate did not alter gall bladder bile SI. 95% confidence limits for the effect of sodium acetyl salicylate on SI were +0.03 and -0.05.We conclude that (a) sodium acetyl salicylate does not lower SI of gall bladder bile in man; (b) an adequate fall in SI for gallstone dissolution can be achieved with a reduced dose (8 mg kg-' day-') of chenic acid given at bedtime with a low cholesterol diet.

show abstract

Enzymatic determination of cholesterol in bile

Cited by 156 publications

References 4 publications

Taurohyodeoxycholic acid protects against taurochenodeoxycholic acid-induced cholestasis in the rat

Taurohyodeoxycholic acid protects against taurochenodeoxycholic acid-induced cholestasis in the rat

Fasting gall bladder volume and lithogenicity in relation to glucose tolerance, total and intra-abdominal fat masses in obese non-diabetic subjects

Effect of sodium acetyl salicylate on cholesterol saturation of fasting gall bladder bile, with and without chenic acid.

Contact Info

Product

Resources

About