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PubMed1991

Plasma glucagon concentration in cirrhosis is related to liver function but not to portal-systemic shunting, systemic vascular resistance, or urinary sodium excretion.

We tested the hypothesis that increased plasma glucagon concentration resulting from portal-systemic shunting or liver dysfunction causes arterial vasodilation and thereby stimulates sodium retention in cirrhosis. Twenty-seven studies were performed in patients with alcoholic liver disease, 11 of whom had ascites. Liver function was quantitated as the elimination rate of antipyrine, caffeine, and stable isotopes of cholic acid administered both orally (2,2,4,4-2H) and intravenously (24-13C). Portal-systemic shunt fraction was calculated as the ratio of the intravenous and oral clearances of the isotopes of cholic acid. Cardiac output was measured by using Doppler echocardiography. Plasma glucagon concentration was increased in patients with ascites when compared with that in patients without ascites (474 +/- 180 pg/ml vs 245 +/- 120 pg/ml, p = 0.0007) but was unrelated to urinary sodium excretion, heart rate, mean arterial pressure, cardiac output, and systemic vascular resistance (r = -0.48, 0.35, -0.13, 0.18, and 0.22, respectively). Plasma glucagon concentration correlated with the half-lives of all model compounds (r = 0.58, p = 0.002; r = 0.62, p = 0.0008; r = 0.62, p = 0.001; and r = 0.64, p = 0.0005; for caffeine, antipyrine, oral and intravenous cholic acid, respectively) but not with shunt fraction (r = 0.14). Increased plasma glucagon concentration in cirrhosis is probably a result of diminished hepatic clearance. However, increased plasma concentration of glucagon does not appear to cause a hyperdynamic circulatory state or sodium retention.

Glucagon↗

PubMed1989

Effects of some poorly digestible carbohydrates on bile acid bacterial transformations in the rat.

The effects of ingestion of poorly digestible carbohydrates on bacterial transformations of cholic acid and beta-muricholic acid were studied in rats fed on increasing levels of lactose, lactulose, amylomaize or potato starches. Each level was given for 3 weeks and, at the end of each dietary treatment, bile acid faecal composition was analysed and a group of six rats was killed every 4 h during 24 h to determine the amounts of fermented carbohydrate and fermentation characteristics (caecal pH, volatile fatty acids (VFA) and lactic acid concentrations). Fermentation of carbohydrates decreased caecal pH and enhanced caecal VFA and lactic acid concentrations. Irrespective of the poorly digestible carbohydrate, the variation of bacterial transformation always occurred in the same way: the bacterial transformation of beta-muricholic acid into hyodeoxycholic acid was the first to disappear, while omega-muricholic acid formation increased; second, cholic acid transformation decreased and finally all bile acid transformations were strongly affected. There was a significant correlation between bile acid transfer and the minimal caecal pH in vivo. This effect of pH was similar in vitro. To determine whether the levels of bacteria which transformed bile acids were modified, rats fed on the highest amounts of poorly digestible carbohydrates were introduced into isolators and carbohydrate feeding was stopped. Caecal pH recovered its initial value but bile acid transformations remained changed, suggesting that the intestinal microflora were modified by ingestion of fermentable carbohydrates.

Animals↗

PubMed1982

Bile salt metabolism in the first year of life.

Bile salt metabolism was examined in 12 infants (ages 7 weeks to 10 months) who had recovered from protracted infantile diarrhea. Cholic acid kinetics were measured with the isotopic dilution technique. Cholate pool size was 938 +/- 89 mg/m2 (means +/- S.E.), synthetic rate was 478 +/- 52 mg/m2/day, and the fractional turnover rate was 0.537 +/- 0.060 day -1. Estimated chenodeoxycholate pool size was 607 +/- 103 mg/m2. similar cholic acid pool sizes were previously observed in older children; however, the synthetic and turnover rates were significantly lower, p less than 0.05 and 0.025, respectively. A significant inverse relationship between age and fractional turnover rate (r = -0.577, p less than 0.05) was observed in the first 10 months of life. Fasting serum cholylglycine measured by radioimmunoassay was significantly higher (p less than 0.01) in infants than in children. Peak postprandial concentrations were higher in infants than in older children. Accelerated hepatic bile salt synthesis rapidly increases the size of small pools at birth. Intraluminal bile salt concentrations concurrently increase, thereby normalizing fat solubilzation. Slow maturation of intestinal transport mechanisms may result in normal cycling of bile salts by 3 to 7 months of age. Persistent immaturity of hepatic uptake and/or excretion of bile salts leads to intrahepatic retention of a portion of the pool, with resultant regurgitation into the serum during the first months of life.

Adult↗

PubMed1983

Bile acid metabolism in hypothyroid subjects: response to substitution therapy.

Bile acid kinetics and biliary lipid composition were determined in ten hypothyroid patients before and after treatment with L-thyroxine. Hypothyroid patients had normal synthesis rates of cholic acid and chenodeoxycholic acid. Hormone treatment, which lowered plasma cholesterol by about 35%, stimulated the formation of chenodeoxycholic acid by about 40% but did not significantly change the synthesis of cholic acid or total primary bile acids. The mean relative biliary concentration of deoxycholic acid was decreased from 30% to 19% and that of chenodeoxycholic acid was concomitantly increased. Cholesterol saturation of bile was decreased by treatment in six of the patients, but the mean value before treatment (135 +/- 13%) was not significantly different from that obtained after treatment (108 +/- 9%). It is suggested that the hypocholesterolaemic effect of thyroid hormones is not primarily due to an increased degradation of cholesterol to bile acids. Similar to what is observed in heterozygous familial hypercholesterolaemia, the defective receptor mediated degradation of plasma low density lipoproteins in hypothyroidism is thus apparently associated with a quantitatively normal catabolic rate of cholesterol to bile acids.

Aged↗

PubMed1982

[Conjugated bile acids and sulphated glycolithocholic acid in the serum of healthy probands (author's transl)].

Using commercially available radioimmunoassays, bile acids were measured in the serum of 378 healthy probands. The following values were found: conjugated cholic acid 0.36 +/- 0.38 mumol/l (95% percentile 1.28 mumol/l) (CG-radioimmunoassay from Abbot); sum of the various conjugated cholanic acids 2.8 +/- 1.58 mumol/l (95% percentile 5.98 mumol/l) (CBA-radioimmunoassay from Becton-Dickinson); sulphate glycolithocholic acid 0.57 +/- 0.33 mumol/l (95% percentile 1.23 mumol)l) (SLCG-radioimmunoassay from Abbot). The values showed a normal logarithmic distribution. No sex-specific differences were found between similar age groups of the 207 male and the 171 female probands. In 50 probands, serum concentrations were followed over a period of 3 hours after a standardized meal. Conjugated cholic acid showed a 5-fold postprandial increase, compared with the concentrations measured in fasting probands. In 48% this maximum was reached within 60 minutes, in 32% within 2 hours, and in 20% within 3 hours. The concentrations of sulphate glycolithocholic acid were subject to only slight postprandial variations, which did not appear until the second or third hour.

Adult↗

PubMed1975

Identification and quantitation of cholanoic acids in hepatic and extra-hepatic tissues of rat.

Tissues of rats were examined for the presence of cholanoic acids. Quantitation of extraction, deconjugation, and isolation were verified by use of radioactive standards. Identification was made by thin layer and gas liquid chromatographic comparison to standards and mass spectrometry. All tissues examined were found to contain several conjugated cholanoic acids. Liver contained primarily cholic acid and peripheral tissues primarily dihydroxy compounds, mainly hyodeoxycholic acid.

Adipose Tissue↗

PubMed1996

Bifidobacteria strain behavior toward cholesterol: coprecipitation with bile salts and assimilation.

Resting cells and growing cells of bifidobacteria strains exhibited an ability to remove cholesterol in the presence of bile salts. In resting cell assays, the removed cholesterol was precipitated in the presence of cholic acid at pH values lower than 5.4. However, this precipitated cholesterol was redissolved when the pellets were washed with phosphate buffer, pH 7, and no cholesterol was found in the cells. It appears that this precipitation is a transient phenomenon. In the case of growing cells, the removed cholesterol was partially recovered when cells were washed with phosphate buffer, pH 7, while the remaining cholesterol was extracted from the cells. Cultured in the presence of radiolabeled free or esterified cholesterol, bifidobacteria strains were able to assimilate esterified cholesterol. It is concluded that the removal of cholesterol from the growth medium by bifidobacteria strains is due to both bacterial assimilation and precipitation of cholesterol.

Bifidobacterium↗

PubMed2002

Postprandial changes in serum unconjugated bile acid concentrations in healthy beagles.

OBJECTIVE: To investigate postprandial changes in serum concentrations of unconjugated bile acids in healthy Beagles. ANIMALS: 7 healthy Beagles. PROCEDURE: Blood samples were obtained from dogs at regular intervals up to 8 hours after consumption of a meal. Serum concentrations of 5 unconjugated bile acids were determined at each time point, using gas chromatography-mass spectrometry with selected ion monitoring. RESULTS: Total serum unconjugated bile acid concentration was significantly increased, relative to baseline values, at 360, 420, and 480 minutes after feeding. Unconjugated cholic acid was significantly increased at 360, 420, and 480 minutes. The proportion of total unconjugated bile acids represented by cholic acid was significantly increased at 240 to 480 minutes. Deoxycholic acid was significantly increased at 360 and 420 minutes. Chenodeoxycholic acid was significantly increased at 360 to 480 minutes. Lithocholic acid was significantly increased at 180 minutes, whereas no significant changes in ursodeoxycholic acid were detected at any time point. CONCLUSIONS AND CLINICAL RELEVANCE: Healthy Beagles had significant increases in serum concentrations and changes in the profile of unconjugated bile acids after a meal. These increases persisted > 8 hours, indicating that prolonged withholding of food is necessary to avoid the risk of a false-positive diagnosis when assessing serum unconjugated bile acid concentrations in dogs.

Animals↗

PubMed1996

Bile acids produce a generalized reduction of the catalytic activity of cytochromes P450 and other hepatic microsomal enzymes in vitro: relevance to drug metabolism in experimental cholestasis.

In bile duct-ligated male rats, there is a reduction of total hepatic microsomal cytochrome P450 (P450) levels and of NADPH-cytochrome P450 reductase (P450-reductase) activity, but the changes in activity of individual microsomal enzymes are nonuniform. We have proposed that the initial effect of cholestasis on microsomal proteins is a non-specific reduction caused by bile acid-mediated destruction, whereas the disproportionate lowering of male-specific P450 enzymes results from secondary down-regulation of some cytochrome P450 (CYP) genes. We report herein the results of experiments to test the first part of this hypothesis, at least as indicated by enzyme inhibition. Hepatic microsomal fractions from normal male rats were incubated at 37 degrees C with increasing concentrations of a range of bile acids selected for their varying physicochemical properties. The endpoints were catalytic activity of three individual CYP proteins, CYP 2A1 (measured as testosterone 7 alpha-hydroxylase activity), 2C11 (testosterone 2 alpha-hydroxylase and 16 alpha-hydroxylase) and 3A2 (testosterone 6 beta-hydroxylase), and the non-CYP enzymes, steroid 17 beta-dehydrogenase and P450-reductase. With 0.25 mmol/L cholic acid, a concentration exceeded in serum following bile duct ligation, there was a significant reduction in the activity of all enzymes at 4 h. Cholic acid-mediated inhibition was dose-dependent and there was no difference in inhibitory activity towards the male sex-dependent CYP 2C11 and 3A2 and the non-sex-dependent CYP 2A1 and other microsomal enzymes. Taurocholic acid was twice as potent an inhibitor as unconjugated cholic acid, the respective apparent I50 values being approximately 0.6 mmol/L compared with approximately 1.2 mmol/L. The dihydroxy bile acids, chenodeoxycholic acid and deoxycholic acid, were also more potent inhibitors than cholic acid, exhibiting I50 values in the range of 0.3-0.5 mmol/L, but the monohydroxy bile acid, lithocholic acid, was the most potent inhibitor (I50 approximately 0.2 mmol/L). Thus, the inhibitory potential of bile acids towards microsomal enzymes was inversely related to their extent of hydroxylation, while taurine conjugation enhanced the inhibitory potential of cholic acid. These data confirm the potential of bile acids to inhibit the activity of microsomal enzymes in livers of bile ductligated rats and indicate that such changes can occur with concentrations of bile acids that are physiologically relevant. Further, the results are consistent with the proposal that the disproportionately greater reduction of the male sex-dependent CYP, 2C11 and 3A2, is not explained by a destructive mechanism.

Animals↗

PubMed1989

Effects of oleic acid and bile salts on canine villous motility.

The effects on canine villous motility of mucosal Tyrodes solution containing oleic acid (10 mM) and/or either taurocholic or cholic acid (15 mM) in the presence or absence of IV atropine (1 mg/kg) was used to assess the neural mediation of the effects of luminal nutrients. Villous motility was measured over 12 min periods by in vivo videomicroscopy of segments of jejunum. Neither bile salt had effects alone but villous motility increased after oleic acid was added to taurocholate and decreased after oleic acid was added to cholate. Villous motility increased when taurocholate and oleic acid were present initially and returned to control levels when removed. Villous motility was not affected by cholate and oleic acid but villous motility decreased when they were removed from the Tyrodes solution. Atropine blocked the increase in villous motility caused by taurocholate and oleic acid. Bile salts can modify the effect of oleic acid on villous motility and a cholinergic step is involved in the stimulation of motility.

Animals↗

PubMed1984

3'-Isothiocyanatobenzamido[3H]cholate, a new affinity label for hepatocellular membrane proteins responsible for the uptake of both bile acids and phalloidin.

Substitution of the hydroxyl group on C7 of cholic acid by a benzamido group leads to a derivative with inhibiting quality for the inward transport of both bile acids and phallotoxins by isolated liver cells. The tritiated isothiocyanate derivative was prepared (3'- isothiocyanatobenzamido [3H]cholate, [3H] IBCA ) with a specific activity of 70-80 mCi/mmol. The latter compound was used for affinity labeling of liver plasma membranes in order to detect chemically modified proteins involved in the transport of bile acids. [3H] IBCA and the noncovalently binding analogs were recognized by the transport system; they inhibited the uptake of both [14C]cholate and of demethyl[3H] phalloin in vitro. Isothiocyanatobenzamidocholate ( IBCA ) was able to protect isolated hepatocytes against phalloidin. In isolated and purified plasma membranes prepared from liver cells [3H] IBCA binds to saturable sites in an irreversible manner. Micromolar concentrations of unlabeled IBCA or millimolar concentrations of natural substrates prevented [3H] IBCA binding in a concentration dependent manner; some other substrates of the transport system also protected liver membranes against chemical modification. Membranes from AS- 3OD hepatoma cells, well known to transport neither bile acids nor phallotoxins, could not be labeled by [3H] IBCA . The major targets of labeling in hepatocellular plasma membranes were polypeptides with molecular mass of 67, 60, 54, 50, and 37 kDa as shown by SDS-polyacrylamide gel electrophoresis (10% acrylamide). The 67 kDa protein could be found in the aqueous phase after phase separation in Triton X-114. The 54 kDa and 50 kDa proteins remained in the detergent phase and can therefore be regarded as integral membrane proteins.

Affinity Labels↗

PubMed1980

Effects of a standardized wheat bran preparation on biliary lipid composition and bile acid metabolism in young healthy males.

The effects of adding bran to the normal diet on biliary lipid composition and bile acid metabolism in a group of young healthy males was studied. A chemically standardized coarse wheat bran product, with serum lipid lowering properties, in a dose of 0.5 kg-1 body weight per day was used. Bran feeding for 4 or 8 weeks did not change biliary lipid and biliary bile acid composition. Faecal bile acid and neutral sterol composition was similar before and after 8 weeks of bran. Bile acid kinetics, measured by double isotope dilution after simultaneous injection of [3H]cholic acid and [14C]deoxycholic acid, showed only minor differences before and during bran ingestion. The most surprising finding was an increase in 7 alpha-dehydroxylation fraction (input of deoxycholic acid divided by synthesis of cholic acid) in six out of seven subjects after 4 weeks of brain and in all four subjects after 8 weeks of bran. In conclusion, the bran product we used is not effective in lowering the biliary cholesterol saturation in healthy young males. Nor does it reduce deoxycholate input in our subjects even after 8 weeks of bran.

Adult↗

PubMed2003

The effects of ursodeoxycholic acid alone and ursodeoxycholic acid plus low-dose acetylsalicylic acid on radiolucent gallstones.

BACKGROUND/AIMS: Mucin, a high molecular weight glycoprotein secreted by the gallbladder and biliary duct epithelium, is a pronucleating agent in experimental and human gallstone disease. Blockage of mucin release with aspirin inhibits the formation of primary gallstones in animal models. The aim of this study was to compare the effects of ursodeoxycholic acid alone and plus low-dose aspirin on dissolution of solitary or multiple gallstones. METHODS: There were three treatment groups comprising 43 patients with cholesterol gallstones: Group I (n=16, 13 females, three males) was given ursodeoxycholic acid (15 mg. kg. day) alone and Group II (n=14, 12 females, two males) was treated with aspirin (100 mg/day) in addition to ursodeoxycholic acid cholic. Group III was a control group of 13 cases (11 females, two males) who were monitored without medical treatment. Stone dissolution rates were evaluated sonographically in all patients at three month intervals during the treatment period. RESULTS: After 12 months of treatment, stone dissolution was found in six (37.5%) of the patients in Group I and six (42.8%) of the patients in Group II. The difference in both treatment groups was significant compared to controls (p<0.05) but there was no significant difference between the two treatment groups (p>0.05). Of the cases in whom dissolution was achieved, all patients had multiple gallstones except for one with a solitary stone in Group I. Gallstones were not dissolved of any subject of group III. CONCLUSIONS: The results showed that ursodeoxycholic acid cholic therapy is more effective in the dissolution of multiple gallstones than of solitary ones. Combination with aspirin did not potentiate the efficacy of ursodeoxycholic acid cholic.

Adult↗

PubMed1987

Effect of dietary ascorbic acid, cholesterol and PCB on cholesterol concentrations in serum and liver in a rat mutant unable to synthesize ascorbic acid.

The effect of ascorbic acid deficiency and excessive ascorbic acid intake on serum and liver levels of cholesterol and lipids was investigated in ODS-od/od (OD) rats fed a normal diet, a cholesterol-containing diet or a polychlorinated biphenyl (PCB)-containing diet. The OD rat is a rat mutant unable to synthesize ascorbic acid. In OD rats, the dietary requirement of ascorbic acid to maintain normal growth and normal levels of cholesterol in serum and liver is about 300 mg of ascorbic acid/kg diet. In control (ODS-+/+) rats that can synthesize ascorbic acid, dietary addition of 0.5% cholesterol and 0.25% cholic acid caused elevation of cholesterol concentrations in serum and liver, elevation of total lipids in liver and reduction of the ratio of high density lipoprotein (HDL) cholesterol to total cholesterol in serum. Dietary addition of PCB (200 mg/kg diet) caused elevation of serum concentration of cholesterol and of the ratio of HDL-cholesterol to total cholesterol in serum. In OD rats fed a normal diet, ascorbic acid deficiency slightly elevated serum concentration of cholesterol, elevated liver concentration of cholesterol and reduced the ratio of HDL-cholesterol to total cholesterol in serum; and ascorbic acid excess did not affect serum and liver concentrations of cholesterol and the ratio of HDL-cholesterol to total cholesterol in serum. In OD rats fed a cholesterol-containing diet, ascorbic acid deficiency elevated serum and liver concentrations of cholesterol, and did not affect the ratio of HDL-cholesterol to total cholesterol in serum; and ascorbic acid excess did not affect serum and liver concentrations of cholesterol and the ratio of HDL-cholesterol to total cholesterol in serum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2003

Steroid ring hydroxylation patterns govern cooperativity in human bile acid binding protein.

Human ileal bile acid binding protein (I-BABP) is a member of the intracellular lipid binding protein family. This protein is thought to function in the transcellular transport and enterohepatic circulation of bile salts. Human I-BABP binds two molecules of glycocholate, the physiologically most abundant bile salt, with modest intrinsic affinity but a remarkably high degree of positive cooperativity. Here we report a calorimetric analysis for the binding of a broad panel of bile salts to human I-BABP. The interaction of I-BABP with nine physiologically relevant derivatives of cholic acid, chenodeoxycholic acid, and deoxycholic acid in their conjugated (glycine and taurine) and unconjugated forms was monitored by isothermal titration calorimetry. All bile salts bound to I-BABP with a 2:1 stoichiometry and similar overall affinity, but the derivatives of cholic acid displayed much higher Hill coefficients, a measure of macroscopic positive cooperativity. To test whether the cooperativity was dependent on individual structural features of the bile salt side chain, a series of side-chain-extended bile salts that lacked a hydrogen bond donor or acceptor at C-24 were chemically synthesized. These synthetic variants exhibited the same energetic and cooperativity profile as the naturally occurring bile salts. Our findings indicate that cooperativity in bile salt-I-BABP recognition is governed by the pattern of steroid B- and C-ring hydroxylation and not the presence or type of side-chain conjugation.

Binding Sites↗

PubMed2000

The peroxisome proliferator-activated receptor alpha (PPARalpha) regulates bile acid biosynthesis.

Fibrates are a group of hypolipidemic agents that efficiently lower serum triglyceride levels by affecting the expression of many genes involved in lipid metabolism. These effects are exerted via the peroxisome proliferator-activated receptor alpha (PPARalpha). In addition, fibrates also lower serum cholesterol levels, suggesting a possible link between the PPARalpha and cholesterol metabolism. Bile acid formation represents an important pathway for elimination of cholesterol, and the sterol 12alpha-hydroxylase is a branch-point enzyme in the bile acid biosynthetic pathway, which determines the ratio of cholic acid to chenodeoxycholic acid. Treatment of mice for 1 week with the peroxisome proliferator WY-14,643 or fasting for 24 h both induced the sterol 12alpha-hydroxylase mRNA in liver. Using the PPARalpha knockout mouse model, we show that the induction by both treatments was dependent on the PPARalpha. A reporter plasmid containing a putative peroxisome proliferator-response element (PPRE) identified in the rat sterol 12alpha-hydroxylase promoter region was activated by treatment with WY-14,643 in HepG2 cells, being dependent on co-transfection with a PPARalpha expression plasmid. The rat 12alpha-hydroxylase PPRE bound in vitro translated PPARalpha and retinoid X receptor alpha, albeit weakly, in electrophoretic mobility shift assay. Treatment of wild-type mice with WY-14,643 for 1 week resulted in an increased relative amount of cholic acid, an effect that was abolished in the PPARalpha null mice, verifying the functionality of the PPRE in vivo.

Animals↗

PubMed1981

Cofactor requiremets for 7 alpha-dehydroxylation of cholic and chenodeoxycholic acid in cell extracts of the intestinal anaerobic bacterium, Eubacterium species V.P.I. 13708.

The characteristics of 7 alpha-dehydroxylase, a bile acid-biotransforming enzyme, were determined using dialyzed cell extracts of Eubacterium sp. V.P.I. 12708. 7 alpha-Dehydroxylase was induced by cholic acid in this organism. Induction by cholic acid resulted in the differential synthesis of at least five new polypeptides with molecular weights of 77,000, two at 56,000, 27,000 and 23,500, as determined by both one and two-dimensional sodium dodecyl sulfate polyacrylamide gel electrophoresis. The relative molecular weight of 7 alphs-dehydroxylase activity was estimated by anaerobic Bio-Gel A 1.5 M gel filtration chromatography to be 114,000. NAD+ was the only cofactor to consistently stimulate 7 alpha-dehydroxylase activity in dialyzed cell extracts. The specific activity increased 4- to 6-fold with either cholic or chenodeoxycholic acid as a substrate in the presence of NAD+. NAD+ was also required for the reduction of the delta 6-intermediate to deoxycholic acid. Other pyridine or flavin nucleotides were ineffective cofactors when added alone. Saturation kinetics for NAD+ with cholic or chenodeoxycholic acid as substrates were hyperbolic, and Lineweaver-Burk plots yielded apparent Km values of 0.13 mM and 0.006 mM, respectively. Similar kinetics were obtained with cholic acid giving an apparent Km of 25 microM. The substrate saturation curve for chenodeoxycholic acid 7 alpha-dehydroxylation indicated substrate inhibition at high concentrations of chenodeoxycholic acid (greater than 50 microM). These studies show that 7 alpha-dehydroxylase is an inducible enzyme and requires NAD+ as a cofactor in this bacterium.

Bile Acids and Salts↗

PubMed1995

Effect of colectomy with ileo-anal anastomosis on the biliary lipids.

Total colectomy with ileo-anal anastomosis is an effective treatment for ulcerative colitis and familial adenomatous polyposis. The absence of the colon and the coexistence of bile acid malabsorption may increase bile lithogenicity, but data on biliary lipid composition in patients with this operation is lacking. Our aim was to assess bile lithogenicity, bile composition and mass of biliary lipids within the gallbladder. We studied 11 patients with total colectomy and ileo-anal anastomosis and 16 healthy controls. We measured the percentage composition of conjugated bile acids and the masses within the gallbladder of the three main biliary lipids. This method, in contrast with measurement of cholesterol saturation index, can determine the cause of bile lithogenicity in terms of absolute modifications of the biliary lipids. There was no difference in the cholesterol saturation index between patients and controls. Colectomy patients had reduced masses of all three biliary lipids (medians and ranges, mmol): cholesterol 0.11 (0.03-0.24) vs. 0.36 (0.02-0.96), P < 0.02; bile acid 1.62 (0.75-5.21) vs. 3.95 (1.27-8.70), P < 0.01; phospholipids 0.35 (0.07-0.69) vs. 1.14 (0.14-3.00), P < 0.002. They also had reduced per cent deoxycholic acid: 3.8 (0.0-27.6) vs. 17.4 (6.4-44.7), P < 0.005, and increased percent cholic acid: 44.9 (23.3-71.4) vs. 34.3 (19.2-57.9), P < 0.05. We conclude that, despite having bile acid malabsorption, patients with colectomy and ileo-anal anastomosis have a normal cholesterol saturation index, caused by a concomitant reduction in the masses of all three biliary lipids. The reduced per cent biliary deoxycholic acid may help explain the reduced cholesterol and phospholipid masses in these patients. Total colectomy with ileo-anal anastomosis does not seem to predispose to the formation of cholesterol gallstones.

Adult↗