ライフサイエンスコーパス: bile

1 e apical surface that is normally exposed to bile.

2 ngeal, bronchial, and colonic mucosa but not bile.

3 bile concentration 10 mM) and altered (pH 6, bile 1 or 10 mM) intestinal conditions with different pa

4 ile acid metabolism, leading to intrahepatic bile accumulation in SCD mouse liver.

5 Excessive fecal bile acid (BA) loss causes symptoms in a large proportio

6 ydrolases (BSHs) are the gateway enzymes for bile acid (BA) modification in the gut.

7 s suppression was recently shown to decrease bile acid (BA) synthesis, thus preventing the developmen

8 We found that the secondary bile acid 3beta-hydroxydeoxycholic acid (isoDCA) increas

9 ndent transporter, plays the leading role of bile acid absorption into enterocytes, where bile acids

10 Lupin cotyledons were fractionated and bile acid adsorbing activities were investigated using i

11 nce included those from glycerophospholipid, bile acid and acylcarnitine metabolism.

12 esigned to integrate sensors that respond to bile acid and anhydrotetracycline (aTc), including one c

13 oDCA, suggesting an interaction between this bile acid and nuclear receptor.

14 ed with glycine betaine and L-carnitine, and bile acid and tryptophan metabolism are associated with

15 s are delivered to basolateral side by ileal bile acid binding protein (IBABP) and then released by o

16 tion scores of 3 metabolic pathways, primary bile acid biosynthesis, fatty acid biosynthesis, and bio

17 The gut microbiota and bile acid content were determined in faeces from 35 preg

18 noclostridium, higher microbial capacity for bile acid conversion, and low abundance of some species

19 both plasma and adipose tissue, such as the bile acid derivative deoxycholic acid and the microbiome

20 high-affinity P395(4) or the semisynthesized bile acid derivative INT-777(1,3) at 3 angstrom resoluti

21 Bile acid diarrhoea (BAD) is a common disorder resulting

22 of tropifexor (LJN452), the most potent non-bile acid FXR agonist currently in clinical investigatio

23 discovery of a novel chemical series of non-bile acid FXR agonists based on a tricyclic dihydrochrom

24 xenobiotic metabolism (e.g., Cyp1a4), lipid/bile acid homeostasis (e.g., Lbfabp), and oxidative stre

25 axis that regulates hepatic cholesterol and bile acid homeostasis.

26 thermore, the specific transport pathways of bile acid in enterocytes are described and the recent fi

27 mproved CCS calibration for phospholipid and bile acid isomers.

28 cers limit our ability to modulate secondary bile acid levels in the host.

29 The endogenous bile acid lithocholic acid (LCA) inhibits NAPE-PLD activ

30 Bile acid malabsorption (BAM) was identified in patients

31 Whether bile acid metabolism is abnormal in MS is unknown.

32 ng microbiome properties or restoring normal bile acid metabolism may prevent or slow the progression

33 t inflammation/permeability and dysregulated bile acid metabolism observed in opioid-exposed mice.

34 idence for a novel resilience gene along the bile acid metabolism pathway.

35 fecal microbiota, assessed the expression of bile acid metabolism regulators and examined the immunop

36 We demonstrate that bile acid metabolism was altered in MS and that bile aci

37 ry to loss of canalicular bile transport and bile acid metabolism, leading to intrahepatic bile accum

38 duced from carbohydrate, protein, lipid, and bile acid metabolism.

39 dly influenced by the microbiome's impact on bile acid metabolism.

40 a butyrate producing genus, and Bilophila, a bile acid metabolizing genus.

41 l resulted in significant alterations in the bile acid metabolome with little to no changes in gut mi

42 high-throughput screen designed to identify bile acid mimetics we uncovered nonsteroidal small molec

43 The dysregulation of IL-23 pathways and bile acid pathways may be key to the development of WD-a

44 ed "enterohepatic recycling", only 5% of the bile acid pool (~3 g in human) is excreted in feces, ind

45 ss of canalicular bile transport and altered bile acid pool.

46 ete pathway to two central components of the bile acid pool.

47 virus infection in the proximal gut involves bile acid priming of type III interferon.

48 trout-derived chemicals, amino acids, and a bile acid produced potent responses.

49 ere we demonstrate that hepatic JNK controls bile acid production.

50 ties, which correlated with changes in serum bile acid profile.

51 Here we identify G-protein-coupled bile acid receptor 1 (GPBAR1) as a selective regulator o

52 lability by activating the G protein-coupled bile acid receptor 1 (GPBAR1, also called TGR5).

53 tory effect is in part dependent on the TGR5 bile acid receptor.

54 om MS brain tissue, we noted the presence of bile acid receptors on immune and glial cells.

55 distinct regional expression profiles of key bile acid receptors that regulate the type III interfero

56 te dehydrogenase and elevating enterohepatic bile acid recirculation are promising new approaches for

57 mitochondrial respiration and enterohepatic bile acid recirculation due to improvement of endoplasmi

58 tein levels, thereby promoting enterohepatic bile acid recirculation, leading to activation of bile a

59 tural features of GPBAR that are involved in bile acid recognition and allosteric effects, but also s

60 We repurposed the FDA-approved bile acid sequestrant cholestyramine, which we show bind

61 We determined that treatment with the bile acid sequestrant sevelamer reversed the liver injur

62 aluate the efficacy and safety of IW-3718, a bile acid sequestrant, as an adjunct to PPI therapy.

63 Supplementation with a bile acid sequestrant, cholestyramine, prevented WD-indu

64 Bile acid sequestrants are orally administered polymers

65 Bile acid sequestrants interrupt intestinal reabsorption

66 e acid metabolism was altered in MS and that bile acid supplementation prevented polarization of astr

67 log of fibroblast growth factor 19, inhibits bile acid synthesis and regulates metabolic homeostasis.

68 nabled by aldafermin-mediated suppression of bile acid synthesis and, in particular, decreases in tox

69 Bile acid synthesis plays a key role in regulating whole

70 erum FGF19, and reduced C4 (reflecting lower bile acid synthesis).

71 deficiency alters cholesterol metabolism and bile acid synthesis, conjugation, and transport, resulti

72 n, which may be useful in disorders in which bile acid toxicity is implicated.

73 The ileal apical sodium-dependent bile acid transporter (ASBT) is crucial for the enterohe

74 Apical sodium-dependent bile acid transporter (ASBT), an ileal Na(+)-dependent t

75 patic recycling, especially the mechanism of bile acid uptake by ASBT, and the development of bile ac

76 rett's cell, CP-C and CP-A, to the oncogenic bile acid, deoxycholic acid (DCA), for 1 year.

77 egulates the expression of genes involved in bile acid, fat, sugar, and amino acid metabolism.

78 ith the biliary toxin, biliatresone, and the bile acid, glycochenodeoxycholic acid.

79 tudied the in vitro effects of an endogenous bile acid, tauroursodeoxycholic acid (TUDCA), on astrocy

80 acid uptake by ASBT, and the development of bile acid-based oral drug delivery for ASBT-targeting, i

81 drug delivery for ASBT-targeting, including bile acid-based prodrugs, bile acid/drug electrostatic c

82 the recent finding of lymphatic delivery of bile acid-containing nanocarriers is discussed.

83 ile acid/drug electrostatic complexation and bile acid-containing nanocarriers.

84 th two virus strains (a pandemic GII.4 and a bile acid-dependent GII.3 strain).

85 urrently no approved therapies for NASH, the bile acid-derived FXR agonist obeticholic acid (OCA; 6-e

86 promoting TFEB nuclear translocation, while bile acid-induced fibroblast growth factor 19 (FGF19), a

87 affolds that bind and inhibit TcdB through a bile acid-like mechanism.

88 aviruses within hours of infection through a bile acid-pDC-IFN signaling axis, which affects viremia,

89 acid recirculation, leading to activation of bile acid-responsive genes in the intestinal ileum to au

90 Veillonella may be a bile acid-sensitive bacteria whose enrichment is enabled

91 rgeting, including bile acid-based prodrugs, bile acid/drug electrostatic complexation and bile acid-

92 am regulatory factor analysis implicated the bile acid/farnesoid X receptor in some of these processe

93 characterized despite extensive research on bile-acid chemistry(14).

94 Here we examined the role of bile acids (BA) in western diet (WD)-induced loss of col

95 We investigated the role of bile acids (BAs) and the gut microbiome in the pathogene

96 Bile acids (BAs) are important regulators of metabolism

97 Primary bile acids (BAs) are synthesized within hepatocytes and

98 Bile acids (BAs) comprise heterogenous amphipathic chole

99 Accumulation of bile acids (BAs) may mediate development of necrotizing

100 Bile acids (BAs) play essential roles in facilitating li

101 Bile acids (BAs), metabolites in the gut, signal nutrien

102 on disorder resulting from increased loss of bile acids (BAs), overlapping irritable bowel syndrome w

103 y bile acids (SBAs) are derived from primary bile acids (PBAs) in a process reliant on biosynthetic c

104 Secondary bile acids (SBAs) are derived from primary bile acids (P

105 Bile acids act on several receptors such as Farnesoid X

106 Elevated bile acids activated pregnane X receptor, which was suff

107 Serum bile acids and autotaxin activity remained unchanged.

108 tatins abolish the insulinotropic effects of bile acids and on the other hand, FXR determines the lev

109 Interactions between bile acids and plant-based materials, and the related fe

110 Furthermore, stool bile acids and propionate are elevated, especially in no

111 ngs thus establish an etiologic link between bile acids and PTB, and open an avenue for developing et

112 Bile acids are cholesterol metabolites that can signal t

113 bile acid absorption into enterocytes, where bile acids are delivered to basolateral side by ileal bi

114 The absorbed bile acids are delivered to the liver via portal vein.

115 Intestinal bile acids are known to modulate the germination and gro

116 Bile acids are recognized as signaling molecules regulat

117 Furthermore, fecal bile acids are reduced in pregnant Fxr(-/-) mice.

118 Bile acids are synthesized from cholesterol in the liver

119 mportantly, aberrant systemic circulation of bile acids can greatly disrupt metabolic homeostasis.

120 m gamma-glutamyltransferase, C4, and primary bile acids decreased significantly at week 24 in both ci

121 most abundant metabolites are the secondary bile acids deoxycholic acid (DCA) and lithocholic acid (

122 More importantly, bile acids dose-dependently induce PTB with minimal hepa

123 ofile the microbiome, metabolic products and bile acids in BAD.

124 In addition to suggesting a role for bile acids in C. difficile pathogenesis, these findings

125 icile Here we describe a role for intestinal bile acids in directly binding and neutralizing TcdB tox

126 Many strains deconjugate primary bile acids in in vitro assays, and a Clostridium scinden

127 t can reduce itch and lower endogenous serum bile acids in intrahepatic cholestasis of pregnancy (ICP

128 examine the implications of lower levels of bile acids in MS, we studied the in vitro effects of an

129 tic steatosis, liver biochemistry, and serum bile acids in patients with NASH.

130 s are orally administered polymers that bind bile acids in the intestine, forming nonabsorbable compl

131 strate that cholestasis, the accumulation of bile acids in the liver, fails to promote liver injury i

132 We find that bile acids induce TcdB into a compact "balled up" confor

133 Muricholic acids and several other bile acids inhibited Nape-pld with potency similar to th

134 lin release and prevents positive effects of bile acids on beta cell function.

135 s a G protein-coupled receptor for secondary bile acids placed at the interface between liver sinusoi

136 de a comprehensive analysis of how secondary bile acids produced by unique members of the microbiota

137 e show that individual primary and secondary bile acids reversibly bind and inhibit TcdB to varying d

138 Bile acids such as chenodeoxycholic acid (CDC) acutely e

139 ic acid (p < 0.0001), with more unconjugated bile acids than women with untreated ICP or uncomplicate

140 with CD had reduced microbial metabolism of bile acids that partially normalized during EEN.

141 included the amino acid conjugations of host bile acids that were used to produce phenylalanocholic a

142 ostridium scindens strain produces secondary bile acids via dehydroxylation.

143 ajor components of the recirculating pool of bile acids(4); the size and composition of this pool are

144 levels of 7alpha-hydroxy-4-cholesten-3-one, bile acids, alanine and aspartate aminotransferases, and

145 n (aromatic compounds, secondary or sulfated bile acids, and benzoate) and estrogen metabolites, as w

146 Serum lipids, glucose, insulin, bile acids, and endothelial and inflammation biomarkers

147 fatty acids, converting primary to secondary bile acids, and facilitating colonization resistance aga

148 with targeted quantification of fecal SCFAs, bile acids, and functional microbial genes.

149 cluding those involving amino acids, lipids, bile acids, and uremic toxins.

150 P), a disorder characterised by raised serum bile acids, are at increased risk of developing gestatio

151 strants interrupt intestinal reabsorption of bile acids, decreasing their circulating levels.

152 lanced levels of short-chain fatty acids and bile acids, improved gut barrier integrity and increased

153 tubulo-toxic factors, such as endotoxins and bile acids, might mediate parenchymal renal injury in pa

154 d transcription factor that, upon binding of bile acids, regulates the expression of genes involved i

155 pitomized by the bacterial transformation of bile acids, which creates a complex pool of steroids(8)

156 ked by gut microbiome-mediated hydrolysis of bile acids.

157 crucial for the enterohepatic circulation of bile acids.

158 of inflammation, fatty acid metabolism, and bile acids.

159 chia, and Enterococcus and increased primary bile acids.

160 n biomarkers HDL and ApoA1, as well as total bile acids.

161 hesis and, in particular, decreases in toxic bile acids.

162 cycle, tocopherol, polyamine metabolism, and bile acids.

163 ophobic interactions between polyphenols and bile acids.

164 rvesiculation is lost upon pre-adaptation to bile and antimicrobial peptides, indicating the importan

165 herapy was poor with a coverage of bacterial bile and blood culture isolates in 51 and 69%, respectiv

166 In this study, we analysed how results of bile and blood cultures and patient data can be used for

167 KAPE), and other enteric pathogens to resist bile and how these interactions can impact the sensitivi

168 phospholipid present in high proportions in bile, behaved similarly, with ~75% reduction in micellar

169 ile flow, which is normally expressed in the bile canaliculi in the liver.

170 oholic fatty liver disease, such as decay of bile canaliculi network and ductular reactions.

171 r that extrudes phosphatidylcholine into the bile canaliculi of the liver.

172 The organoids organized a functional bile canaliculi system, which was disrupted by cholestas

173 hepatic organoids; development of functional bile canaliculi was imaged live.

174 ng revealed impaired bile secretion into the bile canaliculi, which was secondary to loss of canalicu

175 atic in vitro digestion under healthy (pH 7, bile concentration 10 mM) and altered (pH 6, bile 1 or 1

176 ts than frozen strawberries, while increased bile contents in intestinal fluid (fed state) facilitate

177 stem developmental disorder characterized by bile duct (BD) paucity, caused primarily by haploinsuffi

178 Hepatocyte, fibrotic lesion, and bile duct (cancer) were classified and HCA mapping showe

179 The role of common bile duct (CBD) stenting in the establishment of bile st

180 y mesenchymal cells (PMCs) that surround the bile duct after cholestatic and hepatocellular injury.

181 fluid (n = 5, collected before surgery) and bile duct brushings (n = 2) were analyzed for translocat

182 well as in matched pancreatic cyst fluid and bile duct brushings.

183 Cholangiocarcinoma (CCA) is a bile duct cancer that originates in the bile duct epithe

184 ll as in PDACs and pancreatic cyst fluid and bile duct cells from the same patients.

185 illary neoplasms (IOPNs) of the pancreas and bile duct contain epithelial cells with numerous, large

186 by which mutations in ciliary genes lead to bile duct developmental abnormalities is not understood.

187 ghts into the regulatory network controlling bile duct differentiation and morphogenesis during liver

188 he number of patients diagnosed with chronic bile duct disease is increasing and in most cases these

189 is a bile duct cancer that originates in the bile duct epithelium.

190 Although laparoscopic common bile duct exploration (LCBDE) deals with gallstones and

191 ies not only the tubular architecture of the bile duct in three dimensions, but also its barrier func

192 on of CVS contributes to the stable rates of bile duct injuries in LC.

193 ell Polarity signalling components following bile duct injury and promote the formation of ductular s

194 in the development of cholestatic liver and bile duct injury in mouse models of sclerosing cholangit

195 Bile duct injury was induced by the administration of 3,

196 Benign biliary stricture occurs secondary to bile duct injury, anastomotic narrowing, or chronic infl

197 on in the portal region, without evidence of bile duct injury.

198 iary damage/senescence and liver fibrosis in bile duct ligated and Mdr2(-/-) (alias Abcb4(-/-)) mice

199 In livers of mice subjected to bile duct ligation (BDL) and in cultured activated hepat

200 erize the detailed hemodynamics of mice with bile duct ligation (BDL)-induced liver fibrosis, by moni

201 cholestatic liver injury and fibrosis after bile duct ligation (BDL).

202 s, rats and mice with liver fibrosis (due to bile duct ligation [BDL] or administration of carbon tet

203 s were studied 4-weeks after sham surgery or bile duct ligation and were injected with saline or LPS

204 In beta-Arr2-deficient mice, bile duct ligation injury (BDL) led to significantly red

205 A 4-week bile duct ligation model was used to develop cirrhosis w

206 Mice underwent bile duct ligation or were fed 3,5-diethoxycarbonyl-1,4-

207 jury through carbon tetrachloride treatment, bile duct ligation, and 0.1% 3,5-diethoxycarbonyl-1,4-di

208 ly impedes liver fibrosis induced by CCl(4), bile duct ligation, and more importantly NASH.

209 receptors in Mdr2KO mice resulted in reduced bile duct mass and hepatic fibrosis.

210 C presence or activation; large intrahepatic bile duct mass, inflammation and senescence; and fibrosi

211 and show that ANKS6 function is required for bile duct morphogenesis and cholangiocyte differentiatio

212 s a neonatal liver disease with extrahepatic bile duct obstruction and progressive liver fibrosis.

213 ium, focal bile duct stricture formation and bile duct obstruction.

214 hological signs of inflammation/fibrosis and bile duct obstruction.

215 h Ranson and APACHE II scores and markers of bile duct obstruction.

216 e conventional surgical management of common bile duct stones (CBDS).

217 apillary growth of biliary epithelium, focal bile duct stricture formation and bile duct obstruction.

218 iver, lymph nodes, pancreas and extrahepatic bile duct with potential for recurrence and persistent l

219 vessels were dissected after division of the bile duct without a porto-caval shunt.

220 the azygos vein, right hepatic vein, common bile duct, and superior mesenteric artery.

221 cterised by a chronic and destructive, small bile duct, granulomatous lymphocytic cholangitis, with t

222 , morphological changes were observed in the bile duct, including ductal epithelial proliferation, mi

223 reduces the amount of scar formed around the bile duct, without reducing the development of the pro-r

224 Here, we report on a bile duct-on-a-chip that phenocopies not only the tubula

225 e characteristics of precancerous lesions of bile duct.

226 chanistically, we showed that Yap/Taz mutant bile ducts degenerated, causing cholestasis, which stall

227 nes by bile salts during passage through the bile ducts to the gut(4).

228 uman cholangiocytes, epithelial cells lining bile ducts, were cultured as polarized epithelia in a Tr

229 nd monocytes were found to be located around bile ducts.

230 nd monocytes were found to be located around bile ducts.

231 ed the immunopathological characteristics of bile ducts.

232 tion of the intrahepatic and/or extrahepatic bile ducts.

233 export pump, a transporter that facilitates bile flow, which is normally expressed in the bile canal

234 bile salts into the canalicular lumen drives bile formation and promotes biliary cholesterol and phos

235 al microscopy revealed a mixing of blood and bile in the sinusoids, and validated the presence of inc

236 sfully resist the bactericidal conditions of bile, including bacteria that do not normally cause gast

237 Given that pathogen exposure to bile is an essential component to gastrointestinal trans

238 Bile is one of the most innately bactericidal compounds

239 (DGE), postpancreatectomy hemorrhage (PPH), bile leak, blood loss, reoperation, readmission, oncolog

240 indo >=3 complications, LOS, POPF, DGE, PPH, bile leak, reoperation, readmission, or oncologic outcom

241 astric emptying (21.2% vs 22.4%, P = 0.930), bile leakage (4.5% vs 3.1%, P = 0.686), intra-abdominal

242 more safety and longer survival, blood loss, bile leakage, and morbidity should be reduced.

243 atic fistula, postpancreatectomy hemorrhage, bile leakage, delayed gastric emptying, wound infection,

244 bidity due to decreases in blood loss>2L and bile leakage.

245 l of small intestine, appendix, gallbladder, bile, liver, and urine.

246 d significantly higher HU values of wall and bile (median value of 33 HU vs. 21 HU and median value o

247 dder wall of more than 31.5 HU, intraluminal bile more than 12.5 HU, and combined wall-lumen HU of mo

248 ow-colored metabolite of heme degradation (a bile pigment), once believed to be toxic, but recently r

249 n, markers for hepatobiliary function (total bile production, biliary bilirubin, and bicarbonate), an

250 njugated and unconjugated BAs existed in non-bile reflux and healthy juice.

251 inically diagnosed as gastritis with/without bile reflux and healthy subjects for BA profiles measure

252 onjugated BAs became prominent components in bile reflux juice, whereas almost equal amounts of conju

253 kers to facilitate diagnosis of pathological bile reflux.

254 yticus and V. cholerae, ToxR is required for bile resistance and virulence, and ToxR is fully activat

255 it that cannot be avoided, understanding how bile resistance mechanisms align with antimicrobial resi

256 e to host-derived antimicrobial peptides and bile, respectively.

257 cretion whereas biliary bile salt output and bile salt composition remains unchanged.

258 In vitro assays to assess inhibition of the bile salt export pump (BSEP), mitotoxicity, reactive met

259 levels, small heterodimer partner (SHP), and bile salt export pump (BSEP).

260 from MYO5B(P663L) piglets had alterations in bile salt export pump, a transporter that facilitates bi

261 1 levels, hepatic HAX-1 deficiency increases bile salt exporter protein levels, thereby promoting ent

262 10a1) with Myrcludex B, is expected to limit bile salt flux through the liver and thereby to decrease

263 Bile salt hydrolase activity was reduced in women with l

264 f the gut through the activity of the enzyme bile salt hydrolase.

265 Gut microbial enzymes, bile salt hydrolases (BSHs) are the gateway enzymes for

266 of alterations in bile salt output, biliary bile salt hydrophobicity, or increased activity of dedic

267 tes within just 4 h, with increasing primary bile salt levels in vitro and using ex vivo microbiota s

268 ensal bacteria modulate primary to secondary bile salt levels to control germination.

269 l and phospholipid excretion whereas biliary bile salt output and bile salt composition remains uncha

270 tion, which is independent of alterations in bile salt output, biliary bile salt hydrophobicity, or i

271 limiting enzyme for the classical pathway of bile salt synthesis.

272 al pathogen Vibrio cholerae by degrading the bile salt taurocholate that activates the expression of

273 Instead, NTCP inhibition shifts hepatic bile salt uptake from mainly periportal hepatocytes towa

274 Disrupting hepatic bile salt uptake, by inhibition of sodium-taurocholate c

275 NTCP inhibition shifts bile salt uptake, which is generally more periportally r

276 t exhibits anti-aggregation activity against bile salt-induced protein aggregation.

277 nd phospholipid molecules to be excreted per bile salt.

278 zed using a fluorescently labeled conjugated bile salt.

279 e complex thermodynamic interactions between bile salts alone or with phospholipids, i.e. mixed micel

280 Trimethylamine, cadaverine, bile salts and amino acids could play a role in the mech

281 Bile salts are secreted into the gastrointestinal tract

282 shed in faeces and stripped of membranes by bile salts during passage through the bile ducts to the

283 le of gastric treatments and the presence of bile salts in the release and bioaccessibility of encaps

284 As drugs and bile salts interact, increasing the absorption of lipoph

285 Active secretion of bile salts into the canalicular lumen drives bile format

286 sing exposure of the canalicular membrane to bile salts linking to increased biliary cholesterol secr

287 nce, exposure of the canalicular membrane to bile salts was increased, allowing for more cholesterol

288 ntial digestion processes using low and high bile salts was ~ 70% and ~ 90%, respectively.

289 erature could influence micellar behavior of bile salts, and in turn whether this affected the biolog

290 Amino acids, primary bile salts, trimethylamine and cadaverine were elevated

291 urocholate (STC) belongs to a major class of bile salts.

292 Intravital imaging revealed impaired bile secretion into the bile canaliculi, which was secon

293 nclusion Bowel abnormalities and gallbladder bile stasis were common findings on abdominal images of

294 ted sludge-filled gallbladder, suggestive of bile stasis.

295 duct (CBD) stenting in the establishment of bile stream in the elderly patients and the ones who are

296 As silver is reportedly excreted in the bile, the half-life of silver was comparable in all ages

297 In bile, these exist as micelles above their critical micel

298 ed with troglitazone for varying periods and bile transport and accumulation were visualized by live-

299 ream targets, leading to loss of canalicular bile transport and altered bile acid pool.

300 , which was secondary to loss of canalicular bile transport and bile acid metabolism, leading to intr