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PubMed1984

Effect of ML-236B (compactin) on biliary excretion of bile salts and lipids, and on bile flow, in the rat.

To assess the importance of de novo cholesterol synthesis for bile salt formation, the effects of ML-236B (an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase) on biliary excretion of bile salts and lipids were studied in rats with permanent catheters in bile duct, heart and duodenum. In rats having their bile diverted continuously for 8 days, duodenal administration of ML-236B (50 mg/kg) caused an immediate transient choleresis, which subsided after 2 h. Concomitant with the choleresis concentrations of bile salt, phospholipid and cholesterol fell, but this decrease was maintained for 6 h. Consequently, ML-236B inhibited biliary output salts and lipids from the second till the sixth hour after injection. The kinetics of biliary excretion of intravenously injected [14C]taurocholate were not affected by ML-236B administration. In rats having their biliary catheter connected to the duodenal catheter, or in rats with prolonged bile diversion but treated with mevalonolactone, ML-236B again caused a transient choleresis (having subsided after 2 h), but now did not affect biliary excretion of bile salts and lipids. It is concluded that (1) ML-236B causes a transient bile salt-independent choleresis, (2) ML-236B depresses excretion of bile salts and lipids by blocking mevalonate synthesis and not by blocking the bile salt or lipid transport, (3) biliary excretions of phospholipids and cholesterol partly depend on excretion of bile salt, and (4) in rats with a prolonged total bile diversion newly formed mevalonate is a major substrate for bile salt synthesis.

Animals↗

PubMed1975

An enzymic method for the determination of the glycine/taurine ratio of conjugated bile acids in bile.

A method is described in which the ratio of the glycine- to taurine-conjugated bile acids (G/T ratio) in bile is determined. After pretreatment of the bile for removal of the lipids, the bile acids are deconjugated enzymically with choloylglycine hydrolase (EC 3.5.1.24). The amino acids taurine and glycine are liberated in this way, after appropriate isolation, taurine and/or glycine are then determined with ninhydrin, enabling the establishment of the G/T ratio. A nearly complete hydrolysis was obtained for 6 conjugated bile acids, while the recovery of these acids when added to hog or ox bile was quantitative. The mean G/T ratio for hog bile, ox bile and human B-bile was 6.3, 2.5 and 2.0, respectively. The amount of total, free and conjugated bile acids can be determined by this method, combined with the 3alpha-hydroxysteroid dehydrogenase technique for bile acid determination described by Iwata and Yamasaki [1]. A high G/T ratio was observed in 3 cases of Crohn's disease in the small bowel, but the extent of deconjugation in B-bile was lower than in duodenal fluid. The determination of the G/T ratio can be complementary to our knowledge of the metabolism of bile salts in certain gastro-intestinal disorders.

Amidohydrolases↗

PubMed1988

Canalicular bile flow and bile salt secretion are maintained in rats with liver cirrhosis. Further evidence for the intact cell hypothesis.

Different aspects of biliary physiology were studied in rat model of liver cirrhosis induced by CCl4/phenobarbitone. We measured bile flow, bile salt secretion, biliary secretion pressure and bile-to-plasma ratios of inert solutes under basal conditions and during infusion of taurocholate (0.4 and 0.8 mumol.min-1.100 g body wt.-1) in 11 cirrhotic and 10 control male Sprague-Dawley rats. Bile flow and biliary bile salt secretion did not differ between the two groups. Analyzing the relationship between bile salt secretion and bile flow, however, we found an increased slope (P less than 0.02) in the cirrhotic animals, suggesting a higher apparent osmotic activity of the bile salts secreted. Maximal biliary secretion pressure was maintained in cirrhotic animals (22.5 +/- 2.5 vs. 25.0 +/- 2.9 cmH2O) in the absence of exogenous bile salt. During taurocholate infusion it decreased to a lesser extent (P less than 0.001) in cirrhotic animals (13.5 +/- 3.4 vs. 19.3 +/- 3.8 cmH2O). Bile-to-plasma ratios of [3H]sucrose and [14C]ferrocyanide were markedly increased in cirrhotic rats. Biliary [14C]erythritol clearance was equal to bile flow in both groups. In the cirrhotic group, the [3H]sucrose bile/plasma ratio was positively correlated with spleen weight (r = 0.744, P less than 0.01), serum concentration of alkaline phosphatase (r = 0.583, P less than 0.05) and basal maximum biliary secretion pressure (r = 0.801, P less than 0.001). We conclude that chronic portal hypertension is associated with increased permeability of the blood/bile barrier. Nevertheless, bile flow and bile salt secretion are maintained in cirrhotic rats, giving support to the intact cell hypothesis for this important hepatocellular function.

Alkaline Phosphatase↗

PubMed1999

Effects of amino acids on bile acid-dependent and independent bile flow in the isolated perfused rat liver.

BACKGROUND/AIMS: Conflicting data on the effects of amino acids on biliary function led us to investigate their interaction with taurocholate in the perfused rat liver model. METHODS: To investigate the influence of amino acids on the bile acid-independent component of bile flow, 12 livers were perfused with (n = 6) and without (n = 6) amino acid addition from t30 min. For the study of bile acid-dependent bile flow, 24 livers were perfused under 8 experimental conditions according to the perfusate taurocholate concentration (12.5, 25, 37.5 or 50 microM) and whether amino acids were or were not added from t30 min. RESULTS: In the absence of taurocholate, amino acids induced a 40% (p<0.01) decrease in bile flow together with an increase in hepatic water content (17.8%, p< 0.05). Thus, amino acids exert an inhibitory effect on bile acid-independent bile flow despite the postulated cell swelling-dependent increase in bile flow. When livers were perfused at various taurocholate concentrations, amino acids induced, in addition to their inhibitory effect on bile acid-independent bile flow, a significant increase in taurocholate apparent choleretic activity (13.2 microl/micromol vs. 10.6 microl/micromol; p = 0.05), while taurocholate intrinsic clearance was significantly decreased (4.5+/-1.2 ml x min(-1) x g(-1) vs. 6.1+/-1.3 ml x min(-1) x g(-1); p<0.01). CONCLUSIONS: These data suggest that at physiological bile acid concentrations amino acids exert an inhibitory effect on both bile acid-dependent and- independent bile flow, whereas at higher taurocholate concentrations this inhibitory effect disappears, probably because of cell swelling-dependent mechanisms.

Amino Acids↗

PubMed1983

Fluorescence high-performance liquid chromatographic determination of free and conjugated bile acids in serum and bile using 1-bromoacetylpyrene as a pre-labeling reagent.

A fluorescence high-performance liquid chromatographic method is described for the determination of free and conjugated bile acids in serum and bile. Free and conjugated bile acids are extracted from serum or bile using a Sep-Pak C18 cartridge and then fractionated on a piperidinohydroxypropyl Sephadex LH-20 column. Free and glycine-conjugated bile acids are labeled with 1-bromoacetylpyrene in acetonitrile using dicyclohexyl-18-crown-6-ether as catalyst. Taurine-conjugated bile acids are hydrolyzed by cholylglycine hydrolase and then derivatized by the same reagent. Derivatized bile acids are separated stepwise on a reversed-phase column (Radial Pak A) using acetonitrile-methanol-water (A) (100 : 50 : 40) and (B) (100 : 50 : 20) as mobile phase. The eluate is monitored by a fluorophotometer at 370 nm (excitation) and 440 nm (emission). Linearities of fluorescence intensities (peak heights) with the amounts of free and conjugated bile acids were obtained between 50 pmol and 200 pmol for free bile acids and between 25 pmol and 100 pmol for glycine-conjugated bile acids, respectively. Recoveries from serum and bile samples are not less than 90%. This method is sensitive, reliable and useful for the simultaneous determination of free and conjugated bile acids in serum and bile.

Bile↗

PubMed1979

Membranes and bile formation. Composition of several mammalian biles and their membrane-damaging properties.

The total content and profile of bile salts and phospholipids are reported for several mammalian biles. Rabbit and guinea-pig biles are characterized by high proportions of conjugated dihydroxy bile salts with respect to trihydroxy bile salts, but contain relatively little phospholipid. Both rabbit and guinea-pig biles exhibit little evidence of hepatic cell damage, even though they are able to cause membrane damage (as evidenced by lysis of human erythrocytes) at low (2--3 mM) concentrations of bile salts; this lytic behaviour is also a property of their predominant bile salts. Addition of phosphatidylcholine to the bile or bile salt is able to decrease the lytic behaviour. Perhaps the most significant observation is that these biles, and their predominant bile salts, are dramatically less lytic towards sheep erythrocytes, indicating that some factor(s) in membrane composition and structure may partly explain the resistance of membranes of the biliary tract to the presence of high concentrations of potentially membrane-damaging bile salts.

Animals↗

PubMed1970

Effects of rose bengal on bile secretion in the rabbit: inhibition of a bile salt-independent fraction.

The authors have studied the influence of rose bengal, and, by comparison, of uranin, on choleresis in the rabbit. Uranin induced an increase in bile flow and a decrease in bile salt concentration in bile. These results are consistent with an osmotic mechanism, as proposed by Sperber (1959). By contrast, rose bengal induced a marked decrease in bile flow and an increase in bile salt concentration. In rose bengal-treated animals (30 mumoles per kilogram body weight intravenously), bile flow was 65% lower and bile salt concentration 95% higher than in control animals studied during the same periods. The relationship between bile flow and bile salt excretion is consistent in the rabbit, with the existence of a bile salt-independent secretion of 60 mg per minute per kilogram body weight, that is, 60% of bile flow. In rose bengal-treated animals, this fraction was only 15 mg per minute per kilogram body weight. It is concluded that rose bengal inhibits the bile salt-independent fraction. Rose bengal, as other phtalein dyes, is excreted by the liver cells. Its effect on the bile salt-independent fraction suggests that this fraction is secreted by the hepatocytes.

Animals↗

PubMed1986

Bile salt related secretion of acid phosphatase in rat bile.

The biliary excretion of bile salts, lysosomal acid phosphatase, and total proteins were studied in rats under different experimental conditions: during bile salt loss through a bile fistula and after loading with exogenous sodium taurocholate. The experimental models were suitable to demonstrate that variations in the excretion of bile salts were associated with those of acid phosphatase output. During bile salt depletion, acid phosphatase output showed a decrease parallel to that of bile salts. Following a single i.v. injection of sodium taurocholate and during its i.v. infusion, a rapid increase of acid phosphatase excretion in bile was seen. The patterns of enzyme outputs observed after administration of sodium taurocholate suggested a bulk discharge in bile of lysosomal contents. The profiles of protein output were similar to those of acid phosphatase suggesting an association between the secretory mechanism of these bile constituents. In contrast to sodium taurocholate, 4-methylumbelliferone, which also increases canalicular bile flow, did not produce changes in the excretory patterns of the bile components studied. Therefore, the results suggested a bile salt related secretion of acid phosphatase in the rat, which may involve protein secretion in bile.

Acid Phosphatase↗

PubMed1989

Relation between biliary glutathione excretion and bile acid-independent bile flow.

Glutathione efflux into bile of the fluorocarbon-perfused isolated rat liver was altered with eight different agents (L-buthionine-[S,R]-sulfoximine, cefamandole, sodium arsenite, phenobarbital, furosemide, nitrofurantoin, aminopyrine, and benzylamine), and correlations were established between bile flow and biliary excretion of 1) glutathione, 2) endogenous bile acids, and 3) glutathione plus bile acids. Biliary efflux of endogenous bile acids was relatively low (0.5-5 nmol.min-1.g liver-1) and was minimally affected by these agents. Biliary glutathione excretion in control livers was between 4 and 9 nmol.min-1.g-1 and in treated livers ranged from 1 to 21 nmol.min-1.g-1. For each of the various interventions, an increase or decrease in glutathione excretion was always accompanied by a change in bile flow in the same direction; however, these changes were not always directly proportional when comparisons were made between treatment groups. Nevertheless, when bile flow (microliter.min-1.g-1; ordinate) was plotted against glutathione excretion into bile for the pooled data, a significant correlation was observed that was adequately described by a straight line: y = 0.071 chi + 0.72 (r2 = 0.62, P less than 0.001). A similar function described the relation between bile flow and the sum of bile acids and glutathione in bile: y = 0.077 chi + 0.55 (r2 = 0.62, P less than 0.001). In contrast, the taurocholate- or glycocholate-induced choleresis had only minimal effects on glutathione efflux. These findings support the hypothesis that glutathione is one of the osmotic driving forces in bile acid-independent bile formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminopyrine↗

PubMed1980

Electron microscope observations on the intrahepatocytic bile canalicules and sequent bile ductules in the crucian, Carassius carassius.

In the hepatic parenchyme of the crucian, Carassius carassius no interhepatocytic bile canaliculi are detected, but each hepatocyte possesses a single intracellular bile canalicule filled with microvilli protruded from the hepatocyte. The intrahepatocytic bile canalicule originates at the neighborhood of the nucleus to extend to the cell surface where it empties into the intraparenchymal biliary passage running in the interhepatocytic space. The pericanalicular cytoplasm contains many small vacuoles which have possible been elaborated in Golgi complexes and may be discharged by emiocytotic mechanism into the canaliculus, suggesting bile secretion in the crucian liver. The intercellular biliary passage consists of the terminal bile ductule composed of two elongated flat epithelial cells enclosing a narrow and twisted lumen in between; the secondary or middle-sized ductule is surrounded by three cuboidal epithelial cells, and the large bile duct by five or more cuboidal cells and a smooth muscle layer. The basal lamina is detected only in the middle-sized ductule and in the large duct. The intracellular bile canalicules attached to the proximal bile ductule by means of the junctional complex are classified into the "terminal" and "side bile canalicules"; they are attached to the proximal end and the lateral wall of the terminal bile ductule, respectively. The ectoplasmic layer bordering the intracellular bile canalicule is rich in microfilaments which partially enter microvilli, and the epithelial cells of the intercellular biliary duct system are also characterized by abundance of microfilaments. These probably contractile cytoplasmic filaments may control or accelerate bile flow through intrahepatic biliary passages. The periductular or periductal cells closely apposed to intercellular bile passages are thought to be mesenchymal cells such as fibroblasts among which histiocytoid elements are intermingled.

Animals↗

PubMed1977

Effects of chronic choleretic infusions of bile acids on the membrane of the bile canaliculus. A biochemical and morphologic study.

To determine whether choleretic infusions of bile acids modified the function or structure of the membrane of the bile canaliculus, sodium taurocholate (NaTc) or dehydrocholate (DHC) was infused into male rats at a rate of 80 mumoles per hour over an 18-hour period. Bile was collected by fistula and phospholipid and cholesterol content was measured in bile, liver homogenates, and isolated liver plasma membranes (LPM) enriched in bile canaliculi. Na+, K+-ATPase, Mg2+-ATPase, 5'-nucleotidase, and alkaline phosphatase activities were also measured in LPM. NaTc infusions enhanced cholesterol and phospholipid output in the bile in association with a significant increase in phospholipid in both LPM and liver homogenate. Although DHC infusions resulted in a comparable excretion of bile acid, phospholipid and cholesterol output in bile did not increase from control values and the concentration of these lipids in LPM and liver homogenate also did not change. However, LPM Na+, K+-ATPase significantly increased after DHC infusions compared to NaTc-infused animals or controls. Neither bile acid altered the activities of Mg2+-ATPase, 5'-nucleotidase, or alkaline phosphatase. Both bile acids increased the diameter of the lumen of the bile canaliculus as assessed by scanning electron microscopy and produced irregularities and outpouchings in the canalicular membrane. Diverticuli and loss of microvilli were most prominent with DHC infusions whereas canalicular side branching and the density of microvilli, either remained unchanged or increased following NaTc infusions. Although the morphologic findings are qualitative, the results of these studies indicate that chronic choleretic infusions of NaTc and DHC have divergent effects, not only on enzyme activities in liver plasma membrane, but on phospholipid composition and 3-dimensional structure. These findings suggest that bile acids may after biliary secretion not only through their osmotic effects, but by modifying lipids and enzymes in the membrane of the bile canaliculus.

Adenosine Triphosphatases↗

PubMed1989

[Bile fractions and bile secretory component of the migrating myoelectric complex in dogs].

In 4 dogs the functional cholecystectomy was performed, then the common bile duct was cannulated and 9 bipolar electrodes were implanted into the stomach and small intestine. During the interdigestive period when the experiments were carried out both bile flow and electric activity of the gastrointestinal tract were monitored under the following conditions: 1) short or long bile depletion periods, 2) intraduodenal infusions of 50 mM sodium taurocholate, sodium taurodeoxycholate or sodium taurochenodeoxycholate, 3) intraduodenal bile infusions. Total bile acid content was determined in bile samples, then both bile acid-dependent (BAF) and bile acid-independent fractions (BAIF) of bile were calculated. The appearance of the bile secretory component was in 65% correlated with phase III of the MMC while the height of its amplitude usually exceeded 100% of the initial value. In all experimental groups the marked increase in BAIF was followed by a slight enhancement of BAF or its absence. Fluctuations of the biliary fractions were determined by a degree of depletion of the systemic bile acid pool. The changes described were more distinct during infusions of dihydroxy bile acids. The results suggest the importance of BAIF in the appearance of the bile secretory component of the MMC.

Action Potentials↗

PubMed1994

Biochemical studies of inherited diseases related to abnormal cholesterol metabolism. II: Absence of unusual C28 and C29 bile acid homologs in bile and urine of sitosterolemia.

Bile acids, bile alcohols and sterols excreted in bile and urine from a patient with sitosterolemia were studied. Glycine- and taurine-conjugated cholic acid, deoxycholic acid and chenodeoxycholic acid were identified as the major constituents of both the bile and urine. Lesser amounts of unconjugated cholic acid and 3 alpha, 7 alpha, 12 alpha, 24-tetrahydroxy-5 beta-cholestan-26-oic acid were found in the bile, but cholic acid was the only unconjugated bile acid in the urine. Relatively high proportions of campesterol and sitosterol compared to cholesterol were excreted in the bile, while cholesterol was the only sterol detected in the urine. Bile alcohols were not detected in the bile, but the following bile alcohols were excreted in the urine as glucurono-conjugates: 5 beta-cholestane-3 alpha,7 alpha,12 alpha,25-tetrol; 27-nor-5 beta-cholestane-3 alpha,7 alpha,12 alpha,24,25-pentol; 5 beta-cholestane-3 alpha,7 alpha,12 alpha,23,25-pentol; 5 beta-cholestane- 3 alpha,7 alpha,12 alpha,24,25-pentol; 5 beta-cholestane- 3 alpha,7 alpha,12 alpha,25,26-pentol. In neither the bile nor urine, were C28 and C29 bile acid homologs detected. Thus, the main route for the excretion of plant sterols in sitosterolemia is thought to be secretion into the bile as neutral sterols.

Bile↗

PubMed1994

Dietary fish oil potentiates bile acid-induced cholesterol secretion into bile in rats.

Recently we demonstrated that dietary fish oil (FO) causes changes in intrahepatic cholesterol transport and hypersecretion of cholesterol into bile in rats (J. Clin. Invest. 88: 943-951, 1991). We have now investigated in more detail the relationship between cholesterol and bile acid secretion in rats with chronic bile diversion fed purified diets supplemented (9% wt/wt) with either FO or corn oil (CO) for 2 weeks. Effects of FO on biliary cholesterol secretion (+ 400% as compared to CO after 14 days) were much more pronounced than previously observed in rats with intact enterohepatic circulation (+50%). Biliary bile acid (+30%) and phospholipid (+120%) secretion were increased to a much lesser extent than that of cholesterol resulting in the formation of bile supersaturated with cholesterol. The biliary cholesterol/bile acid molar ratio was 0.069 and 0.032 in FO- and CO-fed rats, respectively, at noon of day 14. This ratio increased to 0.108 in FO-fed rats at midnight, when bile acid output was maximal, but remained unchanged in CO-fed rats during the day-night cycle. Intravenous administration of taurochenodeoxycholic acid (15 mumol/kg) resulted in a 2-fold increase in bile acid output and a simultaneous 1.6-fold stimulation of cholesterol secretion in both groups, implying that administration of the bile acid induced the secretion of 2-3 times as much cholesterol in FO- than in CO-fed rats. Likewise, administration of bilirubin ditaurate (30 mumol/kg), an inhibitor of bile acid-induced biliary lipid secretion, reduced cholesterol output in both groups by about 50% while bile acid output remained unchanged. It is concluded that, in rats, dietary fish oil increases the disposition of cholesterol into bile by potentiating bile acid-dependent cholesterol secretion, presumably by facilitating the recruitment of bile-destined cholesterol.

Animals↗

PubMedDate not supplied

Bile acid-dependent secretion of alkaline phosphatase in rat bile.

The role of bile acids in the biliary secretion of alkaline phosphatase was studied. Rats with external bile fistulae were drained for 4 hr. After 2 hr, bile acid secretion fell progressively. Alkaline phosphatase secretion also decreased progressively during the period of drainage, suggesting that secretion of the two components was related. Each rat was then given an i.v. infusion of the taurine conjugate of either cholate, chenodeoxycholate, or ursodeoxycholate. Alkaline phosphatase secretion increased in a dose-dependent manner as bile acid secretion was varied over and beyond the physiologic range. Each bile acid affected alkaline phosphatase secretion differently: given at 0.5 mumoles per min per 100 gm, tauroursodeoxycholate caused a 3-fold, taurocholate a 14-fold, and taurochenodeoxycholate a 75-fold increase in enzyme secretion. To determine if these findings might represent elution of canalicular enzyme by bile acids, isolated liver surface membranes were incubated with the bile acids. Like the findings in vivo, taurochenodeoxycholate was strongest and tauroursodeoxycholate weakest in removing alkaline phosphatase from the membrane. Differential centrifugation of liver surface membranes after exposure to bile acids and ultracentrifugation of bile showed that more than half of the enzyme released by the action of bile acids did not sediment at 100,000 g and, thus, could be considered soluble. These results document bile acid-dependent secretion of alkaline phosphatase in rat bile and suggest that the process involves solubilization of both membrane fragments and free enzyme from membranes lining the biliary space.

Alkaline Phosphatase↗

PubMedDate not supplied

Biliary bile acids in the gall-bladder and the common bile duct of patients with anomalous pancreaticobiliary ductal junction.

The high incidence of biliary tract carcinoma in patients with anomalous pancreaticobiliary ductal junction (APBDJ) with or without choledochal cyst (CC) has been well documented. Twenty-two patients with APBDJ were divided into three groups: Group A, four patients not associated with CC and biliary tract carcinoma; Group B, 13 patients with CC but without biliary tract carcinoma; and Group C, five patients with biliary tract carcinoma (four with and one without CC). Profiles of bile acids in the gall-bladder and/or common bile duct were analysed in these patients and compared with those in the control patients with cholecystlithiasis to examine the hypothesis that the levels of deoxycholic acid (DCA) and lithocholic acid (LCA) are elevated in patients with APBDJ because these secondary bile acids are mutagenic. Bile acids were quantified by gas-liquid chromatography. Total bile acid concentration in the gall-bladder bile was significantly lower in any group with APBDJ than that of controls. In the gall-bladder, increased proportion of chenodeoxycholic acid (CDCA) in Group A and B, decreased proportion of DCA in Group B and increased proportion of cholic acid (CA) in Group C were found in bile. In the bile duct, total bile acid concentration and proportion of DCA were significantly low in bile from Group C and decreased proportion of DCA and increased proportion of CDCA were found in bile from Group B. In both the gall-bladder and hepatic bile, proportion of LCA was not significantly different between any intergroups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1981

Sulfated bile acids in serum, bile, and urine of cirrhotic patients before and after portacaval anastomosis.

Sulfated and unsulfated bile acid composition was studied in serum and bile in 10 patients with alcoholic cirrhosis. Samples, collected before and 2 months after portacaval anastomosis, were analyzed using a gaschromatographic method. Mean total serum bile acid levels rose from 32.0 +/- 5.3 (SE) mumol/liter before to 87.4 +/- 13.3 mumol/liter after surgery (P less than 0.005). The increase in serum bile acid levels was significantly only with respect to the unsulfated fraction (22.7 +/- 3.0 mumol/liter to 67.6 +/- 8.1 mumol/liter, P less than 0.005). Thus the percent sulfation of total serum bile acid decreased from 24.6% to 19.2%. The sulfated bile acid fraction comprised mainly chenodeoxycholate both before and after surgery. Percent sulfation of individual bile acids was not modified after portacaval anastomosis. Bile acid sulfates were present in bile only in negligible amounts. The daily urinary excretion of bile acids, studied in 6 patients, increased significantly (P less than 0.05) after surgery, the increase being due only to the unsulfated compounds. Data from this study indicate that in cirrhotic patients no significant changes occur in serum with respect to sulfated bile acids after portacaval anastomosis, despite a definite increase in serum unsulfated bile acid levels. This is likely due to the lack of an efficient enterohepatic circulation of bile acid sulfates.

Adult↗

PubMed1981

Biliary lipid and bile acid composition in insulin-dependent diabetes mellitus. Arguments for increased intestinal bacterial bile acid degradation.

Bile cholesterol saturation and bile acid composition was studied in 12 nonobese male insulin-dependent diabetics and 28 controls. The total bile lipid concentration in the bile rich duodenal aspirate was lower in the diabetics. The bile cholesterol saturation index was lower in the diabetics if calculated according to Thomas and Hofmann, but not if calculated according to Carey's critical tables. A negative correlation was observed between the cholesterol saturation index of the bile of the diabetics and their long-term metabolic control, as measured by the percentage HbA1c. No correlation existed between the saturation index and the metabolic control at the time of bile sampling as measured by serum glucose, beta-hydroxybutyrate, free fatty acids, and triglycerides. There was also a negative correlation between the cholesterol saturation index and the serum cholesterol concentrations. The glycine-taurine ratio of the conjugated bile acids was increased in the diabetics, as was the percentage concentration of secondary bile acids (deoxycholic acid and lithocholic acid). No correlation was found between the metabolic control of the diabetic state and either the glycine-taurine ratio or the percent concentration of secondary bile acids. These results do not favor a higher incidence of cholesterol gallstones in male juvenile-onset insulin-dependent diabetics. The increased glycine-taurine ratio of the conjugated bile acids and the elevated concentration of secondary bile acids may be due to increased bacterial invasion of the small intestine or decreased absorption of bile acids in the terminal ileum in these insulin-dependent diabetics.

Adolescent↗