Biomedical subjects

S Tazuma

Publications and source records attributed to S Tazuma.

At least 37 records · Page 2Linked to original sources

PubMed2000

Factors affecting gallstone recurrence after successful extracorporeal shock wave lithotripsy.

Ninety-six patients treated successively for symptomatic cholelithiasis with extracorporeal shock wave lithotripsy (ESWL) and oral bile acid therapy consisting of ursodeoxycholic acid in daily dosages of 600 mg were prospectively followed for gallstone recurrence for a median of 13 months. Ultrasonography was performed to detect stone recurrence at 3, 6, and 12 months, and then yearly after the termination of therapy. Recurrent stones were found in 17 patients (18%). The cumulative probability of gallstone recurrence was 15.8% at 12 months, 26.1% at 24 months, and 30.7% at 36 months. The probability of stone recurrence over the entire period of observation was not dependent on stone number, whereas the median interval to detection of recurrence was significantly shorter in the patients with multiple stones (2 months) than in those with solitary stones (8 months) (p < 0.05). The rate of impaired gallbladder contractility was higher in patients with recurrence (8/15, 53.3%) when compared with those with no recurrence (15/72, 20.8%) (p < 0.01). Neither age, gender, or stone characteristics predicted stone recurrence. Only one patient with a recurrence reported biliary pain. Of the 15 patients with recurrent stones who opted for further nonsurgical treatment, complete stone disappearance was achieved in 10. Impaired gallbladder function may predict gallstone recurrence after ESWL.

Cholagogues and Choleretics↗

PubMed1999

Partial replacement of bile salts causes marked changes of cholesterol crystallization in supersaturated model bile systems.

Cholesterol crystallization is a key step in gallstone formation and is influenced by numerous factors. Human bile contains various bile salts having different hydrophobicity and micelle-forming capacities, but the importance of lipid composition to bile metastability remains unclear. This study investigated the effect of bile salts on cholesterol crystallization in model bile (MB) systems. Supersaturated MB systems were prepared with an identical composition on a molar basis (taurocholate/phosphatidylcholine/cholesterol, 152 mM:38 mM: 24 mM), except for partial replacement of taurocholate (10, 20, and 30%) with various taurine-conjugated bile salts. Cholesterol crystallization was quantitatively estimated by spectrophotometrically measuring crystal-related turbidity and morphologically scanned by video-enhanced microscopy. After partial replacement of taurocholate with hydrophobic bile salts, cholesterol crystallization increased dose-dependently without changing the size of vesicles or crystal morphology and the rank order of crystallization was deoxycholate>chenodeoxycholate>cholate (control MB). All of the hydrophilic bile salts (ursodeoxycholate, ursocholate and beta-muricholate) inhibited cholesterol precipitation by forming a stable liquid-crystal phase, and there were no significant differences among the hydrophilic bile-salt species. Cholesterol crystallization was markedly altered by partial replacement of bile salts with a different hydrophobicity. Thus minimal changes in bile-salt composition may dramatically alter bile lipid metastability.

Bile Acids and Salts↗

PubMed1999

Transcytotic vesicle fusion is reduced in cholestatic rats: redistribution of phospholipids in the canalicular membrane.

Cholestasis, which affects phospholipid trafficking, therefore would be expected to alter canalicular membrane phospholipid composition and fluidity, as well as fatty acid composition of membrane phospholipid. These alterations may affect transcytotic vesicle fusion and would be expected to cause variety of cholestatic phenomena. The aim of this study was to determine the effect of cholestasis on transcytotic vesicle fusion. Sprague-Dawley rats with extrahepatic and intrahepatic cholestasis were prepared by bile duct ligation (6 hr or three days) and phalloidin infusion (0.4 mg/kg body weight), respectively. Liposomes of phosphatidylserine/phosphatidylcholine were labeled with octadecyl rhodamine B chloride. Fusion of liposomes to canalicular membrane vesicle preparations from cholestatic and control rats was induced by the addition of calcium. The degree of fusion was evaluated by measuring the increase in rhodamine fluorescence. Membrane phospholipid content also was analyzed. Rates of liposomal fusion to membranes from cholestatic rats were decreased compared to controls. The saturated/unsaturated and saturated/polyunsaturated fatty acid ratios were increased in membrane phosphatidylcholine and decreased in membrane sphingomyelin from cholestatic rats. Cholesterol/phospholipid ratios were increased. Thus, in the presence of cholestasis, a redistribution of phospholipid species within canalicular membranes is associated with decreased transcytotic vesicle fusion. Cholestasis likely decreases membrane fluidity. The regulation of phospholipid species within hepatocellular membranes may play an important role in intrahepatic lipid transport.

Animals↗

PubMed1999

Partial characterization of mechanisms of cytoprotective action of hydrophilic bile salts against hydrophobic bile salts in rats: relation to canalicular membrane fluidity and packing density.

Bile salts regulate the subselection of phosphatidylcholine species secreted into bile and thereby modulate bile metastability. The aim of this study was to determine whether bile salts alter phosphatidylcholine species of the canalicular membrane, and if they do, to clarify whether the cytoprotective action of hydrophilic bile salts is associated with modulation of phosphatidylcholine composition in cell membrane bilayers. Bile salt-pool-depleted rats were infused intravenously with sodium taurocholate at a constant rate (200 nmol/min/100 g body wt) for 2 hr, followed by infusion of either sodium tauroursodeoxycholate, sodium tauroalphamuricholate, or sodium taurobetamuricholate (200 nmol/min/100 g) for 2 hr. Biliary outputs of cholesterol and phosphatidylcholine and phosphatidylcholine hydrophobicity in bile and subcellular fractions were determined. The cytoprotective action of hydrophilic bile salts was determined by the release of canalicular membrane-localizing enzymes (alkaline phosphatase, leucine aminopeptidase) into bile. Tauroursodeoxycholate, taurobetamuricholate, and tauroalphamuricholate decreased the release of these enzymes when compared to values under taurocholate infusion. Bile phosphatidylcholine hydrophobicity was also decreased by the bile salts, whereas the cholesterol/phosphatidylcholine ratio was increased. In contrast, phosphatidylcholine hydrophobicity in the canalicular membrane was increased by these three bile salts. In conclusion, hydrophilic bile salts promote biliary secretion of relatively hydrophilic phosphatidylcholine secretion into bile, and consequently phosphatidylcholine hydrophobicity in canalicular membranes increased. Such an alteration in phosphatidylcholine species within canalicular membrane enhances its lateral packing density with less fluidity, and this may account, in part, for the cytoprotective action of hydrophilic bile salts against hydrophobic bile salts.

Animals↗

PubMed1999

Role of bile salt hydrophobicity in distribution of phospholipid species to carriers in supersaturated model bile solutions.

BACKGROUND: Phospholipid species modulate cholesterol-holding capacity and, therefore, regulate bile metastability. METHODS: In this study, we investigated the effect of bile salt hydrophobicity on the distribution of phospholipids among lipid particles in supersaturated model bile solutions (total lipid concentration, 9 g/dL; taurocholate/phospholipid ratio 3.0, cholesterol saturation index 1.3), by using gel permeation chromatography. RESULTS: With an increase of bile salt hydrophobicity in the elution buffer, the uptake of cholesterol and phospholipids into bile salt micelles was increased, associated with an increased cholesterol/phospholipid molar ratio of the vesicles. In contrast, there was an inverse correlation between the hydrophobicity of the phospholipid species in the vesicles and that of bile salts in the elution buffer, suggesting that hydrophobic bile salts induced preferential uptake of hydrophobic phospholipids into bile salt micelles, while less hydrophobic phospholipids, with a relatively low cholesterol-holding capacity, remained in the vesicles. CONCLUSIONS: These data indicate that bile salt hydrophobicity regulates vesicular cholesterol metastability by modulating the hydrophobicity of phospholipids in vesicles, as well as the lipid distribution among various biliary lipid particles.

Bile↗

PubMed1999

Effects of bilirubin ditaurate on biliary secretion of proteins and lipids: influence on the hepatic vesicle transport system.

BACKGROUND: Several organic anions cause dissociation of biliary lipid secretion from bile acid secretion (uncoupling). As bile lipids originate from liver microsomes and are transported by carrier proteins and/or transcytotic vesicles, such a reduction of biliary lipid secretion may lead to cytosolic accumulation of vesicles. This study investigated whether bilirubin conjugate, a physiologically important organic anion, caused uncoupling and whether hepatic retention of compounds carried by transcytotic vesicles occurred subsequently, using bilirubin ditaurate, a synthetic commercially available compound. METHODS: Cannulation of the bile duct and femoral vein was done in male Sprague-Dawley rats. Sodium taurocholate was infused intravenously at a constant rate of 100 nmol/min per 100 g bodyweight. Bilirubin ditaurate (50 nmol/min per 100 g bodyweight) was infused concomitantly, followed by periodical bile collection for analysis of lipids, total protein and immunoglobulin A. RESULTS: Biliary bile acid secretion was not changed significantly by infusion of bilirubin ditaurate. In contrast, the secretion of cholesterol, phospholipids and immunoglobulin A was decreased by 57.3, 48.7 and 44.8%, respectively. The biliary cholesterol:phospholipid ratio was increased by 19%. Uncoupling was caused by bilirubin ditaurate and biliary immunoglobulin A secretion was decreased. CONCLUSIONS: As immunoglobulin A is a major protein carried by intrahepatic transcytotic vesicles, uncoupling may involve impairment of intrahepatic vesicular transport. Also, a reduction of immunoglobulin A secretion into bile by organic anion-induced uncoupling may weaken biliary immunity.

Animals↗

PubMed1999

Influence of cholesterol crystallization effector proteins on vesicle fusion in supersaturated model bile.

BACKGROUND: In lithogenic bile, cholesterol-rich vesicles rapidly aggregate and fuse to eventually form cholesterol crystals. This process is modulated by cholesterol crystallization effector substances. In this study, we developed a method for quantitative assessment of vesicle fusion and used it to partly characterize the mechanisms of action of cholesterol crystallization effector proteins. METHODS: Cholesterol:phospholipid (1:1) liposomes were prepared and labelled with octadecyl rhodamine B chloride (R18). Fusion of these liposomes was detected by the increase of R18 fluorescence after incubation with various proteins, such as albumin, concanavalin-A bound glycoprotein, immunoglobulins, apolipoprotein A-I and apolipoprotein B (all at 100 microg/mL). RESULTS: Fusion of cholesterol/phospholipid liposomes was increased by 16 and 14% in the presence of concanavalin-A bound glycoprotein and immunoglobulins, respectively, and decreased by 21 and 9% after addition of apolipoprotein A-I and apolipoprotein B, respectively. The effect of each protein on vesicle fusion was correlated with its hydrophobicity. CONCLUSIONS: These results suggest that nucleation effector proteins modulate the stability of vesicles and, thus, affect cholesterol crystallization. Such modulation is based upon protein-vesicle association, which defines the physico-chemical metastability of vesicular cholesterol.

Apolipoprotein A-I↗

PubMed1999

Fate of residual fragments after successful extracorporeal shock wave lithotripsy.

PURPOSE: The aim of the present study was to investigate the reason residual fragments from upper urinary tract calculi failed to clear after successful extracorporeal shock wave lithotripsy (ESWL). METHODS: Risk factors were analyzed in 161 patients with residual fragments (< or = 4 mm) that had remained for more than 3 months after ESWL. The factors examined in the present study were gender, a history of urolithiasis, the number, location and size of stones, hydronephrosis 3 months after ESWL and bacteriuria before ESWL. The mean follow-up period was 20.0 months (range 6-69 months). RESULTS: The overall stone-free rate was 14.3%. The stone-free rate in patients with multiple stones or hydronephrosis 3 months after ESWL was significantly lower than that in patients without these conditions (P < 0.05 and P < 0.01, respectively). The cumulative non-clearance rate in patients with hydronephrosis was significantly higher than in patients without this condition (P < 0.05). Results of Cox's proportional hazards model indicated that hydronephrosis was the most important and only significant factor for failure to clear of the seven factors investigated (P < 0.05). CONCLUSION: Hydronephrosis was most highly correlated with the fate of residual fragments after ESWL.

Adolescent↗

PubMed1998

Quantitative assessment of comparative potencies of cholesterol-crystal-promoting factors: relation to mechanistic characterization.

The crystallization of cholesterol is affected by various factors in bile. The present study evaluated the relative importance of cholesterol-nucleation-promoting factors and partially characterized the mechanisms of their action. Model biles with an identical relative composition of cholesterol, egg-yolk phosphatidylcholine and taurocholate, except for replacing phosphatidylcholine (5-20%) with dilinoleoyl-phosphatidylcholine or taurocholate (10-30%) with taurodeoxycholate. Cholesterol crystallization was quantitatively assessed spectrophotometrically and morphologically estimated by the laser-scattering diffraction analyser and video-enhanced microscopy in the absence and presence of concanavalin A-binding glycoprotein isolated from human bile. In a series of experiments, lipid distribution among particulate species was determined after isolation by FPLC. In all experiments, cholesterol crystallization was dose-dependently enhanced with a rank order of: concanavalin A-binding glycoprotein > dilinoleoyl - phosphatidyl choline> taurodeoxycholate. No morphological alteration was evident for vesicles and crystals, but the cholesterol/phospholipid ratio in vesicles was increased significantly by replacement with dilinoleoyl-phosphatidylcholine and excess cholesterol. A high proportion of relatively hydrophilic phosphatidylcholine species such as dilinoleoyl-phosphatidylcholine and excess cholesterol in bile cause a redistribution of cholesterol to increase a vesicular cholesterol/phospholipid ratio, eventually promoting cholesterol crystallization, whereas concanavalin A-binding glycoprotein acts via differing mechanisms.

Bile↗

PubMed1998

Extracellular and intracellular regulation of biliary lecithin hydrophobicity.

Bromosulfophthalein and papaverine have been demonstrated to inhibit biliary lipid secretion without affecting secretion of bile salts in normal rats, so-called uncoupling. Bromosulfophthalein inhibits the capacity of intracanalicular bile salt micelles to induce biliary lipid secretion, and papaverine inhibits vesicular transport within the hepatocyte. We compared the effects of bromosulfophthalein and papaverine on biliary lipid secretion in normal Sprague-Dawley rats and Eizai hyperbilirubinuria rats. The fatty acyl chain saturation in biliary lecithin increased during bromosulfophthalein infusion and decreased during papaverine infusion in Sprague-Dawley rats. Bromosulfophthalein had no effect on biliary lipid secretion in Eizai rats, while papaverine induced uncoupling. The degree of fatty acyl chain saturation in biliary lecithin was unchanged during bromosulfophthalein infusion, but decreased with papaverine in Eizai rats. We deduce that selection of biliary lecithin species occurs at various points in the lipid transport pathway at intracellular and intracanalicular sites.

Animals↗

PubMed1998

Bile salt hydrophobicity modulates subselection of biliary lecithin species in rats depleted of bile salt pool.

Although bile salts play an important role in the secretion of biliary lipid, little is known about the relationship between bile salt hydrophobicity and the selection of lecithin species to be secreted into bile. We therefore investigated whether bile salts modulate the selection of biliary lecithin subspecies. Rats that were depleted of the bile salt pool were infused with taurocholate (50, 100, 200, and 400 nmol/min/100 g body weight), taurochenodeoxycholate (25, 50, 100, and 200 nmol/min/100 g body weight), tauroursodeoxycholate (100, 200, 400, and 800 nmol/min/100 g body weight), or taurobetamuricholate (100, 200, 400, and 800 nmol/min/100 g body weight). Bile was collected to analyze bile flow, bile acid output, cholesterol levels, and lecithin levels. The hydrophobic-hydrophilic balance of the bile salts and biliary lecithin species was assessed by determining the retention times during reverse-phase high-performance liquid chromatography. Biliary lecithin secretion rates correlated with the hydrophobicity index of the biliary bile salts administered. Thus, biliary lecithin hydrophobicity increased with increasing bile salt hydrophobicity, whereas the molar cholesterol-lecithin ratio in the bile decreased. In conclusion, bile salt hydrophobicity regulates the selection of biliary lecithin subspecies during biliary secretion and thereby modulates, at least in part, bile cholesterol metastability. Thus, bile salt hydrophobicity accounts for the physicochemical conditions determining bile lipid metastability.

Animals↗

PubMed1998

A combination therapy with simvastatin and ursodeoxycholic acid is more effective for cholesterol gallstone dissolution than is ursodeoxycholic acid monotherapy.

Inhibitors of 3-hydroxy,3-methylglutaryl coenzyme A (HMG-CoA) reductase have been reported to decrease the cholesterol saturation index (CSI) in duodenal bile in humans and to prevent formation of cholesterol gallstones in animal studies. We performed a prospective study to evaluate the role of HMG-CoA reductase inhibitors as gallstone-dissolving agents. Fifty patients with radiolucent gallstones in a gallbladder opacifying at drip infusion cholecystography were treated with either 10 mg/day simvastatin plus 600 mg/day ursodeoxycholic acid (group 1, n=26) or 600 mg/day ursodeoxycholic acid alone (group 2, n=24) for 12 months. The ratio of solitary to multiple gallstone cases was 21:29. Plasma lipid levels were assessed and ultrasonographic examination of the gallbladder was performed at baseline and at 3-month intervals during treatment. Duodenal bile sampling was performed in five patients in each group at baseline and after 12 months of treatment. Plasma cholesterol decreased significantly in group 1 but not in group 2. In solitary gallstone cases, no significant difference in dissolution rates was observed between groups 1 (3 of 9, 33%) and 2 (4 of 12, 33%). In contrast, the dissolution rate in multiple gallstone cases was significantly higher in group 1 (12 of 17, 71%) than in group 2 (3 of 12, 25%) (p < 0.01). Bile cholesterol saturation index was significantly decreased (p < 0.01) but did not significantly differ between the two groups. These results suggest that combination therapy with simvastatin and ursodeoxycholic acid is more effective for cholesterol gallstone dissolution than ursodeoxycholic acid monotherapy in patients with multiple gallstones.

Bile↗

PubMed1998

The comparative potency of cholesterol crystallization-effector proteins in supersaturated model bile systems: association with vesicle transformation.

Various proteins which affect cholesterol crystallization are known to be present in bile, although the relative potency of their action is yet to be established. In this study, we evaluated the comparative potency of nucleating-effector proteins using a recently developed method for quantitative assessment of vesicle transformation in supersaturated model bile systems, to partially characterize mechanisms of their action. Concanavalin A-bound glycoproteins isolated from human gall-bladder bile shortened cholesterol crystallization time by 40% and increased cholesterol growth rate and final crystal mass by 161 and 19%, respectively, when compared to the control. In addition, immunoglobulins isolated from human gall-bladder bile increased cholesterol growth rate by 9%, but showed no significant effect on cholesterol crystallization time and final crystal mass. In contrast, human serum apolipoproteins A-I and B reduced cholesterol growth rate by 26 and 31% and reduced final crystal mass by 12 and 21%, but did not affect cholesterol crystallization time. Gel permeation chromatography revealed that proteins were distributed to both vesicles and bile salt micelles, but that no marked redistribution of lipids was caused by addition of these proteins. Furthermore, no significant difference in crystal structure was observed by video-enhanced contrast microscopy. These results indicate that nucleating-effector substances tested in this study may modulate vesicular cholesterol-holding capacity, thus affecting cholesterol crystallization. Such modulation is based upon the protein-vesicle association which defines the physico-chemical metastability of vesicular cholesterol.

Analysis of Variance↗

PubMed1998

Living related partial liver transplantation for primary biliary cirrhosis--a case report.

An adult living related partial liver transplantation was performed on a 49 year old female with terminal hepatic failure due to primary biliary cirrhosis (PBC). The donor was her 53 year-old sister. A sufficient volume of graft tissue was obtained, which comprised 1.5% of the body weight of the recipient. The recipient had an excellent recovery without any major complications, and was discharged 35 days after the operation. At 15 months after the operation, the patient has shown no signs of rejection while using FK506 and prednisolone as immunosuppressants. The progression of symptomatic PBC can be predicted, and the timing of the transplantation can be easily determined. In addition, the results of liver transplantation for PBC are good. Therefore, adult living related partial liver transplantation is an excellent treatment for primary biliary cirrhosis.

Bilirubin↗

PubMed1997

A quantitative assessment of serum chylomicron by light scattering intensity: application to the intestinal fat absorption test.

A novel fat absorption test to clarify the malabsorption syndrome was developed using a micronephelometric technique and compared with the classic conventional technique using 131I-triolein. An integrity of time-sequential light scattered from chylomicron-related turbidity in serum was determined between 0 and 300 min after butter fat load, being expressed in terms of the light scattering intensity (LSI). A good correlation was obtained between LSI and the serum level of chylomicron-triglyceride determined by an ultracentrifugation technique (r = 0.819, P < 0.001). The maximal LSI was consistently observed at 180 min after administration of a test meal in the normal group (n = 39), whereas the malabsorption syndrome group (n = 35) was distinctly different and could be further classified according to four patterns of LSI changes. In addition, an inverse correlation was found between this fat absorption test and the 131I-triolein absorption test. It was concluded that the micronephelometric technique which does not use a radionuclide is advantageous in its simple and safe evaluation of fat malabsorption syndrome.

Adult↗

PubMed1997

Effect of cholestasis induced by organic anion on the lipid composition of hepatic membrane subfractions and bile in rats.

Several organic anions inhibit the secretion of cholesterol and phospholipid into bile without affecting total bile acid secretion (uncoupling). The uncoupling induced by sulphobromophthalein (BSP) alters the fatty acid composition of biliary lecithin. The purpose of this study was to investigate the relationship between the lipid composition of bile and of liver subcellular membrane fractions during BSP-induced uncoupling. After depletion of the bile salt pool, rats fitted with a bile duct cannulus were infused with sodium taurocholate given either alone or with BSP. Bile was collected and liver microsomes and canalicular membranes were isolated for analysis of lipid composition. In bile, uncoupling increased the cholesterol/phospholipid ratio (C/P ratio) and the saturated/unsaturated fatty acid ratio (S/U ratio) in phosphatidylcholine. The C/P ratio was increased in the canalicular membrane, but the membrane phosphatidylcholine S/U ratio was decreased during uncoupling. In microsomes, the S/U ratio of membrane phosphatidylcholine was slightly increased, but the C/P ratio was unaffected during uncoupling. These results support the hypothesis that an increased secretion of hydrophobic phosphatidylcholine species from the canalicular membrane into bile reduces the proportion of hydrophobic phosphatidylcholine species in the canalicular membrane during uncoupling. The decreased contribution of hydrophobic phosphatidylcholine species may ameliorate the decrease in membrane fluidity resulting from the accumulation of cholesterol in the canalicular membrane and stimulate the synthesis of hydrophobic phosphatidylcholine species in the microsomes.

Animals↗

PubMed1997

Transcytotic vesicle fusion with canalicular membranes is modulated by phospholipid species: implications for biliary lipid secretion.

Phospholipid species modulate bile metastability and the subselection of such species for biliary secretion occurs at the canalicular membrane. In this study, the role of phospholipid head groups and hydrophobic indices in transcytotic vesicle fusion with the canalicular membrane inner leaflet was investigated using rat canalicular membrane vesicles (CMV) and liposomes. The CMV were purified from Sprague-Dawley rat liver, and small unilamellar vesicles (SUV) of phosphatidylserine (PS), phosphatidylcholine (PC) and mixtures of PS/PC (1:1, 2:1 and 4:1) were labelled with 8 mol% of octadecyl rhodamine B chloride (R18). The PC species used in this study were egg yolk PC (EYPC), soybean PC (SBPC), dipalmitoyl PC (DPPC) and dilinoleoyl PC (DLPC). Fusion of SUV with CMV was initiated by the addition of a millimolar concentration of Ca2+ and the degree of fusion was estimated by the increase of R18 fluorescence. Ca(2+)-dependent fusion of SUV consisting of PS, and PS/PC (4:1) with CMV was observed (PS > PS/PC; 4:1), whereas no detectable fusion was evident between CMV and SUV of PC alone or PS/PC (1:1 or 2:1). The rank order of fusibility between CMV and SUV of PS/PC (4:1) containing various PC species was PS/DLPC > PS/SBPC > PS/EYPC > PS/DPPC. The hydrophobic index of PC as determined by high performance liquid chromatography (HPLC) was related closely to liposome fusibility (r = -0.88). These results suggest that transcytotic vesicle fusion with the canalicular membrane inner leaflet is regulated by the phospholipid hydrophobicity of the vesicles.

Animals↗

PubMed1996

Lecithin hydrophobicity modulates the process of cholesterol crystal nucleation and growth in supersaturated model bile systems.

The present study was performed to determine whether the degree of lecithin hydrophobicity regulates bile metastability and, therefore, affects the process of cholesterol crystallization. Supersaturated model bile (MB) solutions were prepared with an identical composition on a molar basis (taurocholate/lecithin/cholesterol, 73:19.5:7.5; total lipid concentration 9 g/dl) except for the lecithin species; egg yolk phosphatidylcholine, soybean phosphatidylcholine, 1-palmitoyl-2-linoleoyl-sn-phosphatidylcholine, dilinoleoyl phosphatidylcholine and dipalmitoyl phosphatidylcholine. Each MB solution was incubated and sequentially examined. Video-enhanced contrast microscopy demonstrated that the rate of vesicular aggregation and fusion correlated with the degree of lecithin hydrophobicity, and that the rate of cholesterol crystal nucleation correlated with the degree of lecithin hydrophilicity. In MBs containing less hydrophobic lecithin, needle-like crystals developed and transformed into mature plate-like crystals, whereas classical plate-like crystals were consistently observed in MBs composed of hydrophobic lecithin. Laser-diffraction particle size analysis demonstrated that the increase in lecithin hydrophobicity enlarged the vesicle dimension, enhancing its cholesterol-holding capacity. Correlation between vesicular cholesterol packing density and lecithin hydrophobicity suggests that the process of bile cholesterol nucleation and growth is regulated, in part, by acyl chain unsaturation in lecithin. Since the composition of biliary lecithins is responsive to dietary manipulations, this study provides new insights into the prevention of cholesterol gallstones.

Bile↗