ライフサイエンスコーパス: bile

1 nal pathogens, to survive in the presence of bile.

2 ng replacement of endogenous bile by a model bile.

3 rategies to mitigate the toxic components of bile.

4 ecting the liver from the harmful effects of bile accumulation, leading to considerable interest in F

5 irment of bile flow, and that leads to toxic bile acid (BA) accumulation in hepatocytes.

6 dicated severe deregulation of intracellular bile acid (BA) homeostasis and activation of cell prolif

7 Bile acid (BA) signaling regulates fatty acid metabolism

8 The identification of the key regulators of bile acid (BA) synthesis and transport within the entero

9 t and microbiota bile acid metabolism, favor bile acid accumulation that contributes to AhR-mediated

10 Hepatic bile acid and lipid content was elevated in WT mice, wit

11 performed a detailed analysis of gallbladder bile acid and lipid metabolism in Tgr5(-/-) mice in both

12 th disruptions also in tryptophan/serotonin, bile acid and lipid metabolism.

13 in CRC, and the decreased expression of the bile acid apical transporter gene Slc10A2, as an effect

14 itive acid blockers, reflux-reducing agents, bile acid binders, injection of inert substances into th

15 of genes involved in cholesterol and primary bile acid biosynthesis including Cyp7a1.

16 sm, lysine biosynthesis and degradation, and bile acid biosynthesis.

17 TGR5 may play a role in determining bile acid composition and in fasting-induced hepatic ste

18 Analysis of gallbladder bile acid composition showed marked increase of taurocho

19 rofiles of serum, liver and adipose tissues, bile acid composition, energy metabolism, and messenger

20 nction in cholecardia so that reducing serum bile acid concentrations may be beneficial against the m

21 is strongly associated with increased serum bile acid concentrations.

22 R inhibits bile acid synthesis and increases bile acid conjugation, transport, and excretion, thereby

23 trolling C. difficile infection, a series of bile acid derivatives have been prepared that inhibit ta

24 on of bile acids prevented the rise in fecal bile acid excretion, changed the bacterial composition o

25 entified a novel series of highly potent non-bile acid FXR agonists that introduce a bicyclic nortrop

26 FXR is also essential for maintaining bile acid homeostasis and prevents the accumulation of b

27 ces fatty acid oxidation, while FXR controls bile acid homeostasis, but both nuclear receptors also r

28 r-delta (PPAR-delta), which is implicated in bile acid homoeostasis.

29 ing myrcludex B had only moderate effects on bile acid kinetics in WT mice, but completely inhibited

30 However, plasma bile acid levels are normal in a subset of NTCP knockout

31 tudies demonstrated a striking deficiency in bile acid levels in malnourished mice that is consistent

32 demonstrated intestinal sensing of elevated bile acid levels in plasma in mice.

33 FP36L1 reciprocally regulate Cyp7a1 mRNA and bile acid levels in vivo.

34 We find that increased bile acid levels suppress expression of proliferator-act

35 etected a 4.6-fold increase in total hepatic bile acid levels, despite the coordinated repression of

36 receptor that acts as a master regulator of bile acid metabolism and signaling.

37 Thus, the ZFP36L1-dependent regulation of bile acid metabolism is an important metabolic contribut

38 Increased levels of microbial bile acid metabolism loci (bsh, baiCD) are consistent wi

39 circulation, as well as host and microbiota bile acid metabolism, favor bile acid accumulation that

40 um indicated alterations in several steps of bile acid metabolism, including hepatic synthesis and re

41 ith control mice, in part because of altered bile acid metabolism.

42 absorption that was consistent with altered bile acid metabolism.

43 er Partner double knockout mice, a model for bile acid overload, display cardiac hypertrophy, bradyca

44 ology, serum liver enzyme, serum and hepatic bile acid profiles, and hepatic bile acid synthesis and

45 gical analysis as well as gut microbiota and bile acid profiling.

46 olic acid (TLCA), a potent G protein-coupled bile acid receptor 1 (GPBAR1) agonist associated with bi

47 Bile acid receptors and transporters were decreased as e

48 In addition, bile acid receptors such as GPR131 (TGR5) and proton-sen

49 expression is significantly associated with bile acid receptors VDR and TGR5 expression.

50 Activation or modulation of bile acid receptors, such as the farnesoid X receptor an

51 As a cellular bile acid sensor, farnesoid X receptor (FXR) participate

52 mittee down-graded recommendations regarding bile acid sequestrant use, recommending bile acid seques

53 ding bile acid sequestrant use, recommending bile acid sequestrants only as optional secondary agents

54 Importantly, intestinal bile acid sequestration with cholestyramine was sufficie

55 plants containing a T-DNA disruption of the bile acid sodium symporter BASS6 show decreased photosyn

56 ely inhibited active transport of conjugated bile acid species in OATP knockout mice.

57 The role of FXR in regulation of bile acid synthesis and hepatic metabolism has been stud

58 Activation of FXR inhibits bile acid synthesis and increases bile acid conjugation,

59 and hepatic bile acid profiles, and hepatic bile acid synthesis and transportation gene expression w

60 to induce FGF15/19, which modulates hepatic bile acid synthesis and uptake.

61 ids activate FXR, which in turn switches off bile acid synthesis by reducing the mRNA levels of bile

62 cid synthesis by reducing the mRNA levels of bile acid synthesis genes, including cholesterol 7alpha-

63 sterol 7alpha-hydroxylase in the alternative bile acid synthesis pathway was reduced.

64 ish rats from humans including vitamin C and bile acid synthesis pathways.

65 tic free cholesterol accumulation, increased bile acid synthesis, decreased biliary cholesterol secre

66 1H4 or farnesoid X receptor [FXR]) regulates bile acid synthesis, transport, and catabolism.

67 sterol mobilization, cholesterol efflux, and bile acid synthesis.

68 are compatible with previous studies of the bile acid system in stroke models.

69 TBI would alter hepatic function, including bile acid system machinery in the liver and brain.

70 e muscarinic agonist carbachol (CCh) and the bile acid taurolithocholic acid 3-sulfate were also anal

71 330672, a selective inhibitor of human ileal bile acid transporter (IBAT), in patients with primary b

72 A transport systems, apical sodium-dependent bile acid transporter and Na(+) -taurocholate cotranspor

73 cholangitis with pruritus, 14 days of ileal bile acid transporter inhibition by GSK2330672 was gener

74 s, such as the ileal apical sodium-dependent bile acid transporter, appear to affect both insulin sen

75 Quantification of bile acid transporter, ASBT-expressing neurons in the hy

76 Hepatic bile acid uptake kinetics were determined in wild-type (

77 , while the regulatory functions of FGF19 in bile acid, glucose and energy metabolism remain intact.

78 , combined with feces replete with lipid and bile acid, indicated a phenotype more akin to that of st

79 expression and activity of genes involved in bile acid, lipid and carbohydrate metabolism, energy exp

80 receptor (FXR) participates in regulation of bile acid, lipid and glucose homeostasis, and liver prot

81 er partner (SHP) are important regulators of bile acid, lipid, and glucose homeostasis.

82 ytryptamine, chloroquine, compound 48/80, or bile acid, was markedly decreased in TDAG8(-/-) mice.

83 Based on our prior studies with the bile acid-activated nuclear hormone receptor farnesoid X

84 The bile acid-activated receptors, nuclear farnesoid X recep

85 We hypothesized that a bile acid-induced ductular reaction (DR) drives fibrogen

86 sion in cardiac cells was able to rescue the bile acid-mediated reduction in fatty acid oxidation gen

87 ociated with augmented caspase 3 activity in bile-acid-induced apoptosis in mouse hepatocytes whereas

88 the potential for therapeutically targeting bile-acid-related pathways to address this growing world

89 Bile acids (BA) are linked to the pathogenesis and thera

90 dy aims to uncover how specific bacteria and bile acids (BAs) contribute to steatosis induced by diet

91 association between sex and gut microbiota, bile acids (BAs), and gastrointestinal cancers.

92 eostasis in Teff cells exposed to conjugated bile acids (CBAs), a class of liver-derived emulsifying

93 dominated by increases in taurine-conjugated bile acids (t-CBAs).

94 While liver, but not sera, total bile acids (TBAs) were increased 75% by this dose, domin

95 Elevated bile acids activate FXR, which in turn switches off bile

96 e and 5-D itch scale, changes in serum total bile acids and 7 alpha hydroxy-4-cholesten-3-one (C4), a

97 ins mediate the hepatic uptake of conjugated bile acids and demonstrated intestinal sensing of elevat

98 Bile acids and epithelial-derived human beta-defensins (

99 mination is triggered in response to certain bile acids and glycine.

100 ing and interplay with the gut microbiota of bile acids and their receptors in meta-inflammation, wit

101 obially modified molecules such as secondary bile acids and unexpected microbial molecules including

102 Bile acids are signaling molecules that coordinately reg

103 These results identify bile acids as important metabolic effectors under condit

104 We conclude that bile acids can differentially regulate colonic epithelia

105 Here we show that excess bile acids decrease fatty acid oxidation in cardiomyocyt

106 Fecal bile acids decreased 2.8-fold, suggesting enhanced intes

107 Bile acids deoxycholic acid and ursodeoxycholic acid dif

108 In recent years, bile acids have emerged as relevant signaling molecules

109 s contribute to hepatic uptake of conjugated bile acids in mice, whereas the predominant uptake in hu

110 sense highly elevated levels of (conjugated) bile acids in the systemic circulation to induce FGF15/1

111 In fecal samples, levels of primary bile acids increased in the placebo group but not in the

112 The gallbladder excretes cytotoxic bile acids into the duodenum through the cystic duct and

113 hain fatty acids) and lack of products (like bile acids or plasmalogens), many peroxisomal defects le

114 geted the synthesis and biliary excretion of bile acids prevented the rise in fecal bile acid excreti

115 We hypothesized that bile acids regulate colonic HbetaD expression and aimed

116 Importantly, bile acids strongly enhance this bacteriocin activity in

117 lasma levels, as well as fecal excretion, of bile acids that is accompanied by distinct changes in gu

118 s a G protein-coupled receptor for secondary bile acids that is highly expressed in monocytes/macroph

119 rrent available data on the relationships of bile acids to NAFLD and the potential for therapeuticall

120 AT) and hepatic conversion of cholesterol to bile acids via the alternative synthesis pathway.

121 ltiple amino acids (AA), AA metabolites, and bile acids were also significantly lower in diabetic ver

122 Moreover, serum bile acids were increased 45.4-fold, consistent with blo

123 ity lipoprotein, triglycerides, cytokines or bile acids were observed.

124 les were collected at baseline and 16 weeks; bile acids were profiled using high-performance liquid c

125 osition of the gut (i.e., the microbiota and bile acids), the transformation of the gastrointestinal

126 nt between groups included free fatty acids, bile acids, and amino acid metabolites.

127 ns in glycolysis/gluconeogensis metabolites, bile acids, and elevated branched chain AA).

128 ted included those involved in metabolism of bile acids, flavonoids, nutrients, amino acids (includin

129 characterized by impairment of excretion of bile acids, leading to elevation of hepatic bile acids.

130 studied the complex interplay between diet, bile acids, sex, and dysbiosis in hepatic steatosis and

131 en source software, include oxidized lipids, bile acids, sphingosines, and previously uncharacterized

132 bile acids, leading to elevation of hepatic bile acids.

133 d inhibition of hepatic uptake of conjugated bile acids.

134 A cycle, amino acids, carnitine, lipids, and bile acids.

135 ith accumulation of TLCA and other secondary bile acids.

136 ritus, hepatic impairment and elevated serum bile acids.

137 homeostasis and prevents the accumulation of bile acids.

138 primarily phospholipids, sphingolipids, and bile acids.

139 the degradation of cholesterol into primary bile acids.

140 be pivotal for hepatic uptake of conjugated bile acids.

141 through enterohepatic recycling pathways of bile acids.

142 th a high concentration (1 mM) of conjugated bile acids.

143 he adsorbed PAHs to Pimphales promelas using bile analysis via fluorescence spectroscopy.

144 We collected bile and blood samples from 50 patients undergoing thera

145 jury through increased albumin loss into the bile and increased intracellular albumin scavenging of r

146 In summary, hepatic ZIP8 reclaims Mn from bile and regulates whole-body Mn homeostasis, thereby mo

147 nscriptional deregulation of a wide range of bile and steroid metabolism genes and development of liv

148 Novel drug targets include the bile BA receptors, farnesoid X receptor and TGR5, the BA

149 entration, with samples digested with 1mM of bile being more susceptible to inhibitory effects of mag

150 hreshold of 9.46 x 10(14) nanoparticles/L in bile best distinguished patients with malignant CBD from

151 riorized, allowing replacement of endogenous bile by a model bile.

152 ave demonstrated that gut pathogens react to bile by adapting their protein synthesis.

153 de, responds to deoxycholate, a component of bile, by altering global gene transcription in a manner

154 e cellular polarity by delimiting functional bile-canalicular structures, forming the blood-biliary b

155 transports bile salts from hepatocytes into bile canaliculi.

156 Bile cannulations were performed and biliary cholesterol

157 in medium with deoxycholate, a component of bile, caused DNA damage consistent with the exposure to

158 oid bioaccessibility was modulated mainly by bile concentration, with samples digested with 1mM of bi

159 nvestigated whether concentrations of EVs in bile could discriminate malignant from nonmalignant CBD

160 The treatment of common bile duct (CBD) disorders, such as biliary atresia or is

161 Algorithms for diagnosis of malignant common bile duct (CBD) stenoses are complex and lack accuracy.

162 l Pkhd1 on the NOD background produces early bile duct abnormalities, initiating a break in tolerance

163 Hepatic artery is the main blood supply to bile duct and lack of adequate HA flow is thought to be

164 Our results demonstrate that syngeneic bile duct antigens efficiently break immune tolerance of

165 tionship to the pathogenesis of human distal bile duct cancer (DBDC).

166 g a risk factor for developing an aggressive bile duct cancer, cholangiocarcinoma, in chronically inf

167 h rare, obstructive jaundice due to external bile duct compression or rupture of the HAA into the bil

168 C) is a rare progressive disorder leading to bile duct destruction; approximately 75% of patients hav

169 missense mutant of Jag1 (Jag1(Ndr)) disrupts bile duct development and recapitulates Alagille syndrom

170 Bile duct differentiation, morphogenesis, and function w

171 RNA sequencing of NOD.Abd3 common bile duct early in disease demonstrates upregulation of

172 our arising from malignant transformation of bile duct epithelial cells.

173 ly indicated in the management of iatrogenic bile duct injuries (IBDI), but occasionally, it becomes

174 ategies to block progression of intrahepatic bile duct injury in patients with BA.

175 The cystic-common bile duct junction was visualized before Calot triangle

176 In this study, cirrhotic bile duct ligated (BDL) rats with PH were treated with I

177 Biliary hyperplasia was induced in rats via bile duct ligation (BDL) surgery, and galanin was increa

178 (HA) and MCs infiltrate the liver following bile duct ligation (BDL), increasing intrahepatic bile d

179 he pathogenesis of liver fibrosis induced by bile duct ligation (BDL).

180 l of acute cholestatic liver injury, partial bile duct ligation (pBDL), with a novel longitudinal bio

181 the cerebral cortex using rat models of HE (bile duct ligation [BDL] and induced hyperammonemia) and

182 th portal hypertension was established using bile duct ligation in rats.

183 f PDGFRalpha in murine carbon tetrachloride, bile duct ligation, and 0.1% 3,5-diethoxycarbonyl-1,4-di

184 er models of chronic liver injury, including bile duct ligation, nonalcoholic steatohepatitis, and ob

185 mice in two separate murine models: CCl4 and bile duct ligation.

186 es (n = 363) were scored for the presence of bile duct loss and assessed for clinical and laboratory

187 Bile duct loss during acute cholestatic hepatitis is an

188 Bile duct loss during the course of drug-induced liver i

189 etary-supplement-associated liver injury had bile duct loss on liver biopsy, which was moderate to se

190 ive factor of poor outcome was the degree of bile duct loss on liver biopsy.

191 Compared to those without, those with bile duct loss were more likely to develop chronic liver

192 uced liver injury with histologically proven bile duct loss.

193 duct ligation (BDL), increasing intrahepatic bile duct mass (IBDM) and fibrosis.

194 Lower survival is also determined by distal bile duct obstruction, Bismuth- Corlette type IV strictu

195 icrog/kg) every 4 days for 28 days exhibited bile duct proliferation and pericholangitis.

196 receptor 1 (GPBAR1) agonist associated with bile duct proliferation.

197 cholangitis via immunization with syngeneic bile duct protein (BDP).

198 ervals (CIs) were determined for the rate of bile duct strictures, incomplete ablation, and tumor rec

199 essively more differentiated hepatocytes and bile duct structures.

200 ommon, but can be an indication of vanishing bile duct syndrome (VBDS).

201 duodenum through the cystic duct and common bile duct system.

202 Bile duct-ligated (BDL) and sham-treated rats were image

203 and demonstrate that ECOs self-organize into bile duct-like tubes expressing biliary markers followin

204 on of mice increased significantly following bile-duct ligation.

205 es biliary hyperplasia and liver fibrosis in bile-duct-ligated (BDL) rats; however, no information ex

206 .019), distal (non-hilar) obstruction of the bile ducts (HR 3.711, P=0.008), Bismuth-Corlette type IV

207 Small and large intrahepatic bile ducts consist of small and large cholangiocytes, re

208 A left hepatectomy was done and dilated bile ducts filled with caseous necrotic material were se

209 and IRE induces sufficient local heating to bile ducts in 24% of ablations.

210 In a separate set of experiments, bile ducts of male Wistar rats were exteriorized, allowi

211 c for hydatid disease, cyst rapture into the bile ducts should be included in the differential diagno

212 Adjacent intrahepatic bile ducts were dilated.

213 oderate to severe (<50% of portal areas with bile ducts) in 14 and mild (50%-75%) in 12.

214 oinflammatory cholangiopathy (disease of the bile ducts) of unknown pathogenesis.

215 ions are present in the canalicular network, bile ducts, and gallbladder.

216 tes, that line intrahepatic and extrahepatic bile ducts, contribute substantially to biliary secretor

217 first and early lesions are in "downstream" bile ducts.

218 shunting may allow improved targeting to the bile ducts.

219 d fibrosis of the intra- and/or extrahepatic bile ducts.

220 extrahepatic biliary tract and intrahepatic bile ducts.

221 We verified the diagnostic performance of bile EV concentration by analyzing samples from the 30 c

222 , we identified a threshold concentration of bile EVs that could best discriminate between patients w

223 L) and canola oil/coffee creamer, at varying bile extract (1 or 8mM) and pancreatin (100 or 990mg/L)

224 linical disorder defined as an impairment of bile flow, and that leads to toxic bile acid (BA) accumu

225 2(-/-) mice showed normal serum liver tests, bile flow, biliary bile salt secretion, fecal bile salt

226 Microbial testing of collected bile fluid in the treatment group was positive in 91.4%.

227 Bile functions as a defensive barrier against intestinal

228 brain approximately gill > liver > plasma > bile >> muscle.

229 ncreased the ratio of muricholate:cholate in bile, inducing a more hydrophilic bile salt pool.

230 The ability of pathogens to respond to bile is remarkably complex and still incompletely unders

231 bile reflux was grouped as normal, yellowish bile lakes and presence of greenish bile lakes.

232 flux (74% yellowish bile lakes, 13% greenish bile lakes).

233 ) had macroscopic bile reflux (74% yellowish bile lakes, 13% greenish bile lakes).

234 ellowish bile lakes and presence of greenish bile lakes.

235 h Phase I and Phase II), occurring mostly in bile, liver and plasma.

236 to the hepatocyte canalicular membrane, and bile Mn levels were increased in ZIP8-LSKO and decreased

237 ferences between cohorts in the frequency of bile or chyle leaks.

238 Here, we investigated whether altering bile/pancreatin concentration influenced potential negat

239 Bile plays an important role in digestion, absorption of

240 monitoring biliary pH, rather than absolute bile production, may be important in determining the lik

241 was caused by a leaky epithelium and reduced bile re-absorption in the intestines.

242 Endoscopically, 20/23 (87%) had macroscopic bile reflux (74% yellowish bile lakes, 13% greenish bile

243 ct of exposure of esophageal cells to acidic bile reflux (BA/A).

244 ejunostomy in reducing macro and microscopic bile reflux and impact on dyspepsia related quality of l

245 Delayed gastric emptying and bile reflux are common concerns in long-term survivors a

246 Microscopic bile reflux index (BRI) was calculated and a score more

247 Mean bile reflux index score was 9.7 (range 1.77-34).

248 All underwent gastroscopy and bile reflux was grouped as normal, yellowish bile lakes

249 e generally regarded as safe to consume, are bile-resistant and can plausibly be modified to produce

250 tually leads to cholestasis, and this causes bile salt (BS)-mediated toxic injury of the "upstream" l

251 Surprisingly, bile salt destabilization of ToxRp enhanced the interact

252 l intrahepatic cholestasis-1 (FIC1), 18 with bile salt export pump (BSEP) disease, and 4 others with

253 r (FXR), small heterodimer partner (SHP) and bile salt export pump (BSEP).

254 The bile salt export pump (BSEP/ABCB11) transports bile salt

255 in HE-iPSCs, resulting in the expression of bile salt export pump.

256 /-)(low) mice, were sensitive to hydrophobic bile salt feeding (0.3% glycochenodeoxycholate); they ra

257 g for genes encoding glyosyltransferases and bile salt hydrolases.

258 Half of the Fut2(-/-) mice showed serum bile salt levels 40 times higher than wt (Fut2(-/-)(high

259 ile flow, biliary bile salt secretion, fecal bile salt loss, and expression of major hepatocellular b

260 loop-that are essential for accessing SM in bile salt micelles.

261 Strategies that alter bile salt pool composition might be developed for the pr

262 The altered bile salt pool stimulated robust secretion of cholestero

263 Hydrophilicity of the bile salt pool, controlled by FXR and FGF15/19, is an im

264 cholate in bile, inducing a more hydrophilic bile salt pool.

265 anced Claudin-2 expression in colon and that bile salt receptors VDR and Takeda G-protein coupled rec

266 normal serum liver tests, bile flow, biliary bile salt secretion, fecal bile salt loss, and expressio

267 nd cytochrome P450 7a1, the key regulator of bile salt synthesis, indicating that elevated serum bile

268 uctal fibrosis, and sensitivity toward human bile salt toxicity.

269 NA-sequencing analysis verified an important bile salt transcriptional profile in S. flexneri 2457T,

270 loss, and expression of major hepatocellular bile salt transporters and cytochrome P450 7a1, the key

271 gical levels of Ca(2+) may result in altered bile salt-induced TcpP protein movement and activity, ul

272 lk composition and structure by inactivating bile salt-stimulated lipase (BSSL) and partially denatur

273 dylcholine aqueous dispersions stabilized by bile salts (BS) under simulated intestinal conditions (p

274 nsive to various environmental cues, such as bile salts and alkaline pH, but how these factors influe

275 study, we define mechanisms of resistance to bile salts and build on previous research highlighting i

276 flexneri 2457T biofilms determined that both bile salts and glucose were required for formation, disp

277 Furthermore, our work confirms that bile salts are important physiological signals to activa

278 re, using NMR and DSF, it was shown that the bile salts cholate and chenodeoxycholate interact with p

279 for formation, dispersion was dependent upon bile salts depletion, and recovered bacteria displayed i

280 le salt export pump (BSEP/ABCB11) transports bile salts from hepatocytes into bile canaliculi.

281 lt synthesis, indicating that elevated serum bile salts in Fut2(-/-)(high) mice were not explained by

282 that exposure of esophageal cells to acidic bile salts induces phosphorylation of the p47(phox) subu

283 terestingly, extended periods of exposure to bile salts led to biofilm formation, a conserved phenoty

284 together, these data suggest a model whereby bile salts or other detergents destabilize ToxR, increas

285 of weak physiological allosteric inhibitors (bile salts) into potent competitive Autotaxin inhibitors

286 M, and its activity requires the presence of bile salts, a class of physiological anionic detergents.

287 mainly from the reduced level of enzymes and bile salts, as well as the higher gastric pH in the infa

288 f the Lab4 probiotic consortium to hydrolyse bile salts, assimilate cholesterol and regulate choleste

289 ce to pepsin and pancreatin and tolerance to bile salts.

290 flexneri strain 2457T following exposure to bile salts.

291 lability by forming insoluble complexes with bile salts/fatty acids, inhibiting micelle formation.

292 e observed within the physiological range of bile salts; however, growth was inhibited at higher conc

293 entration of EVs was significantly higher in bile samples from patients with malignant CBD stenoses t

294 d mitis group isolates were subjected to our bile solubility test (which measures and calculates the

295 Combining the bile solubility test and the MALDI-TOF spectra results p

296 The bile solubility test based on spectrophotometric reading

297 ir resistance to simulated gastric juice and bile solution.

298 In these mice, hREG3A travels via the bile to the intestinal lumen.

299 tantially to biliary secretory functions and bile transport.

300 and a dilated gallbladder containing dilute bile with high bicarbonate concentration.