ライフサイエンスコーパス: bile acid

1 abolite sensing and signaling pathways (e.g. bile acids).

2 acids and derivatives, free fatty acids, and bile acid.

3 primarily phospholipids, sphingolipids, and bile acids.

4 be pivotal for hepatic uptake of conjugated bile acids.

5 the degradation of cholesterol into primary bile acids.

6 ontaining diet for 7 days to sequester their bile acids.

7 rol and accumulation of toxic oxysterols and bile acids.

8 m to maintain homeostasis in the presence of bile acids.

9 through enterohepatic recycling pathways of bile acids.

10 etabolism, despite changes in microbiota and bile acids.

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

12 nthesis of N-(11)C-methyl-taurine-conjugated bile acids.

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

14 d inhibition of hepatic uptake of conjugated bile acids.

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

16 ith accumulation of TLCA and other secondary bile acids.

17 ritus, hepatic impairment and elevated serum bile acids.

18 homeostasis and prevents the accumulation of bile acids.

19 enabled the pulp hydrocolloid to entrap more bile acids (35-38% at a hydrocolloid concentration of 2%

20 d female mouse faeces, and others respond to bile acids absent in mouse faeces.

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

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

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

24 ch encodes the farnesoid X receptor (FXR), a bile acid-activated nuclear hormone receptor that regula

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

26 ds with PET and the (11)C-labeled conjugated bile acid analog [N-methyl-(11)C]cholylsarcosine ((11)C-

27 Thus, changes in bile acid and inflammatory signaling, insulin resistance

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

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

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

31 with nuclear receptor-controlled cholesterol/bile acid and xenobiotic metabolism among the top deregu

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

33 nthesis of N-(11)C-methyl-taurine-conjugated bile acids and biodistribution studies in pigs by PET/CT

34 ICP is characterized by raised serum bile acids and complicated by spontaneous preterm labor

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

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

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

38 ges closely correlated with changes in serum bile acids and levels of the antiinflammatory bile acid

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

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

41 sor of important molecules such as hormones, bile acids and vitamin D.

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

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

44 Serum biochemistries, gallbladder bile acids, and liver sections were examined.

45 matory responses, normalized serum levels of bile acids, and protected mice from liver damage after e

46 to overcome host barriers, including low pH, bile acids, and the innate immune system.

47 PGs, bile acids, and tryptophan metabolites are important med

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

49 Bile acids are known to induce Ca(2+) signals and necros

50 Bile acids are known to induce pathological Ca(2+) signa

51 Bile acids are ligands for G-protein coupled receptors (

52 Bile acids are ligands for the nuclear hormone receptor

53 Bile acids are ligands for the nuclear hormone receptor,

54 Bile acids are signaling molecules that coordinately reg

55 Bile acids are signaling molecules that play a critical

56 Bile acids are steroid-derived molecules synthesized in

57 Bile acids are synthesized from cholesterol and are know

58 bust source of AOS chemosignals and identify bile acids as a class of natural AOS ligands.

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

60 Recent studies have described bile acids as versatile signaling molecules endowed with

61 d by decreased free and conjugated secondary bile acids as well as changes in gut microbiota.

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

63 on of ISs from a routine LC-MS/MS method for bile acid (BA) analysis with a focus on tauro-conjugated

64 n of the effect of GSK2330672 on total serum bile acid (BA) concentrations, serum markers of BA synth

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

66 osing cholangitis (PSC) may involve impaired bile acid (BA) homeostasis.

67 esoid X receptor (Fxr), which is the primary bile acid (BA) sensor, and critical regulator of BA meta

68 Bile acid (BA) signaling regulates fatty acid metabolism

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

70 Bile acid (BA)-binding capacities of in vitro digested s

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

72 Bile acids (BAs) and phospholipids were measured by mass

73 ), which is a hepatocellular transporter for bile acids (BAs) and the receptor for hepatitis B and D

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

75 Bile acids (BAs) have been proposed as potential prurito

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

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

78 tential applications as food emulsifiers and bile acid binders.

79 fine a potentially treatable inborn error of bile acid biosynthesis caused by ACOX2 deficiency.

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

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

82 Accordingly, hepatocytes did not accumulate bile acids but simply facilitated the transport of bile

83 Outside of this role, bile acids can act as cell signaling effectors through b

84 We conclude that bile acids can differentially regulate colonic epithelia

85 rizes recent findings on the influences that bile acids can exert in normal neurological function and

86 ics of hepatobiliary secretion of conjugated bile acids can now be determined by dynamic (11)C-CSar P

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

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

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

90 n of Cyp7a1 and Cyp8b1 normalizes TCA level, bile acid composition, and intestinal cholesterol absorp

91 ransient fetal liver residence, where select bile acid composition, derived from mother and embryo, p

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

93 g to reduced bile acid pool size and altered bile acid composition, with the alpha/beta-muricholic ac

94 holesterol (chromosome 10A2) and serum total bile acid concentration (chromosome 12E) and identified

95 ELF score of 9.8, and highly elevated total bile acid concentration (median, 43.3 mumol/L); 13 of 20

96 Sel1l as a significant determinant of serum bile acid concentration.

97 es accounted for the variance in serum total bile acid concentrations and had pleiotropic effects on

98 After GSK2330672 treatment, serum total bile acid concentrations declined by 50% (95% CI -37 to

99 8 (median reduction: 0.173), and total serum bile acid concentrations decreased from baseline to week

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

101 Strategies to minimize serum bile acid concentrations may reduce the severity of neur

102 diet had significantly increased serum total bile acid concentrations, providing independent confirma

103 is strongly associated with increased serum bile acid concentrations.

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

105 fed a control, cholestyramine-containing, or bile acid-containing diet before azoxymethane (AOM)-indu

106 Spanish plasma bile acid contents were analyzed by liquid chromatograph

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

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

109 Bile acids deoxycholic acid and ursodeoxycholic acid dif

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

111 However, bile acid-elicited signalling events in stellate cells r

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

113 Individual bile acids exhibit repressive activity on SPI-1-regulate

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

115 cids but simply facilitated the transport of bile acids from blood to bile against a measured concent

116 Bile acids function not only as detergents that facilita

117 Finally, we found that bile acids function synergistically to achieve the overa

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

119 The bile acid-FXR interaction regulates bile acid synthesis,

120 Recently, bile acid-FXR regulation has been reported to play an in

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

122 In contrast, non-conjugated bile acids have a robust stimulatory effect only on delt

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

124 gs demonstrate a pivotal function for FXR in bile acid homeostasis and liver protection.

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

126 evels of liver enzymes, liver histology, and bile acid homeostasis were evaluated.

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

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

129 ort has been made to investigate the role of bile acids in diseases outside of those associated with

130 n body composition, markers of inflammation, bile acids in fecal samples, and composition of the inte

131 cy-specific disorder characterised by raised bile acids in foetal-maternal circulation, which threate

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

133 Increased amounts of total and unconjugated bile acids in the faeces of the probiotic-fed mice, toge

134 equestrants are synthetic polymers that bind bile acids in the gut and are used to treat dyslipidemia

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

136 ts suggest that decreased PRDX3 by excessive bile acids in trophoblasts plays a critical role in the

137 ner similar to endogenous taurine-conjugated bile acids in vivo and are thus promising for functional

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

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

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

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

142 s (e.g., certain short-chain fatty acids and bile acids) inhibit SPI-1 expression.

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

144 s techniques showed that SPI-1 repression by bile acids is mediated by posttranslational destabilizat

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

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

147 ne feeding or using Cyp7A1(-/-) mice reduced bile acid levels and delayed AOM-induced neurological de

148 eceptor dramatically increases enterohepatic bile acid levels and jet-lag-induced HCC, while loss of

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

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

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

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

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

154 Total bile acid levels were increased in the cortex of AOM-tre

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

156 After a meal, bile-acid levels increase in the intestine, liver, and a

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

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

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

160 It is possible that in Barrett's patients bile acids may activate NOX5-S and increase reactive oxy

161 source of AOS information, and suggest that bile acids may be mammalian pheromones and kairomones.

162 ring cholestasis, accumulation of conjugated bile acids may occur in the liver and lead to hepatocell

163 In conclusion, circulating bile acids may play a pathological role during hepatic e

164 Bile acid-mediated pancreatic damage can be further esca

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

166 tion of hepatic glucose as well as lipid and bile acid metabolism and detoxification and their potent

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

168 We hypothesized that modulating bile acid metabolism by the gut hormone fibroblast growt

169 ainly responsible for energy homeostasis and bile acid metabolism in the liver.

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

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

172 Dysregulation of bile acid metabolism was also evident in Gpat3-null mice

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

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

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

176 linked to obesity, T cell infiltration, and bile acid metabolism.

177 absorption that was consistent with altered bile acid metabolism.

178 ng independent confirmation linking SEL1L to bile acid metabolism.

179 ated nuclear hormone receptor that regulates bile acid metabolism.

180 cells and thus killing of stellate cells by bile acids might have important implications in acute bi

181 nificantly reduced the stimulatory effect of bile acids on ENaC, suggesting that this site is critica

182 Effects of bile acids on neurological function and disease.

183 d pancreatic acinar cells but the effects of bile acids on stellate cells are unexplored.

184 emonstrate the pathophysiological effects of bile acids on stellate cells in two experimental models:

185 fect of tauroursodeoxycholic acid (TUDCA), a bile acid, on ER stress in MSCs in vitro and in vivo.

186 tabolism and transport, and sulfonylation of bile acids or hydroxysteroids.

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

188 talyzes conversion of cholesterol to primary bile acids) (OR, 1.11; 95% CI, 1.08-1.15; P = 8.84 x 10(

189 droxysteroids and cholesterol-derived sterol bile acids) (OR, 1.17; 95% CI, 1.12-1.21; P = 2.24 x 10(

190 ion of L-arginine (also in rats), caerulein, bile acid, or an AP-inducing diet.

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

192 tty acids pathway, and primary and secondary bile acids pathways.

193 mall heterodimer partner, leading to reduced bile acid pool size and altered bile acid composition, w

194 inal cholesterol absorption by modulation of bile acid pool size and composition, thus leading to inc

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

196 ses of the N-(11)C-methyl-taurine-conjugated bile acids proceeded with radiochemical yields of 61% (d

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

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

199 ngs shed new light on the mechanism by which bile acids promote pancreatic pathology.

200 Several secondary/primary bile acid ratios were also decreased with LF in the disc

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

202 ted a therapeutic potential for this nuclear bile acid receptor in the prevention of diabetic nephrop

203 ile acids and levels of the antiinflammatory bile acid receptor Takeda G protein-coupled receptor 5 (

204 The role of the G-protein-coupled bile acid receptor TGR5 in various organs, tissues, and

205 regulation and role of the G protein-coupled bile acid receptor TGR5, previously shown to be regulate

206 otein receptor 5 (TGR5), a G protein-coupled bile acid receptor, is linked to cAMP and expressed in c

207 Bile acid receptors and transporters were decreased as e

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

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

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

211 ardiac function, we show that elevated serum bile acids reduce cardiac fatty acid oxidation both in v

212 The mechanisms whereby bile acid reflux may accelerate the progression from Bar

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

214 ng through these diverse signaling pathways, bile acids regulate triglyceride, cholesterol, glucose h

215 duce liver injury with associated changes in bile acid regulating genes, leading to an accumulation o

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

217 forts in mapping functional hot spots on the bile acid scaffold, we here demonstrate that the introdu

218 ion channel family, which also includes the bile acid-sensitive ion channel (BASIC).

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

220 Three placebo trials of bile acid-sequestering agents (n = 332, 8-52 weeks) show

221 Bile acid-sequestering agents were commonly associated w

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

223 Bile acid sequestrants are synthetic polymers that bind

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

225 lation of LDL receptor expression (ie, diet, bile acid sequestrants, ileal bypass, and ezetimibe) (be

226 Importantly, intestinal bile acid sequestration with cholestyramine was sufficie

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

228 alyzed how sevelamer alters inflammation and bile acid signaling in NAFLD livers.

229 and increase insulin sensitivity by altering bile acid signaling pathways.

230 rological decline, and molecular analyses of bile acid signaling were performed.

231 own liver tumor promoter that mediates toxic bile acid signaling, inhibits NAFLD-induced hepatocarcin

232 RTC1 also mediates anti-lipogenic effects of bile acid signaling, whereas it is negatively regulated

233 We demonstrated that tauro-conjugated bile acids significantly stimulate ENaC in the alphabeta

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

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

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

237 ic measures such as probiotics, prokinetics, bile acids, statins, and hematopoietic growth factors co

238 Bile acids stimulate ENaC-mediated currents by increasin

239 Importantly, bile acids strongly enhance this bacteriocin activity in

240 nt physicochemical properties of hydrophilic bile acids such as ursodeoxycholic acid, with the distin

241 d amino acids, biogenic amines, fatty acids, bile acids, sugars, and lipids.

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

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

244 dual FXR and TGR5 agonist INT-767 on hepatic bile acid synthesis and intestinal secretion of glucagon

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

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

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

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

249 duced expression of the genes in the classic bile acid synthesis pathway but induced those in the alt

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

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

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

253 1H4 or farnesoid X receptor [FXR]) regulates bile acid synthesis, transport, and catabolism.

254 The bile acid-FXR interaction regulates bile acid synthesis, transport, and cholesterol metaboli

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

256 safely harnessing FGF19 biology to suppress bile acid synthesis.

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

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

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

260 In this study we found that bile acid taurodeoxycholic acid (TDCA) significantly inc

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

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

263 ed with lithocholic acid (LA)-an inexpensive bile acid that exhibits strong binding to beta-cyclodext

264 Many AOS neurons respond selectively to bile acids that are variably excreted in male and female

265 Faecal extracts contain several unconjugated bile acids that cause concentration-dependent neuronal a

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

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

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

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

270 bition of the ileal, apical sodium-dependent bile acid transporter (ASBT), blocks progression of scle

271 The ileal bile acid transporter (IBAT) protein expressed in the di

272 330672, a selective inhibitor of human ileal bile acid transporter (IBAT), in patients with primary b

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

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

275 ndomised controlled crossover trial of ileal bile acid transporter inhibitor, a novel class of drug t

276 m/taurocholate cotransporting polypeptide (a bile acid transporter) as a receptor to enter hepatocyte

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

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

279 uclear factor 4A (Hnf4a), known modifiers of bile acid transporters and metabolic traits.

280 Bile acid treatment caused necrosis predominantly in ste

281 sport plays an important role in the overall bile acid uptake in pancreatic stellate cells.

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

283 lypeptide (NTCP) indicate a Na(+) -dependent bile acid uptake mechanism in stellate cells.

284 rate conventional treatment with the natural bile acid ursodeoxycholic acid (UDCA).

285 Reducing serum bile acids via cholestyramine feeding or using Cyp7A1(-/

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

287 nthesis of N-(11)C-methyl-taurine-conjugated bile acids was developed and used to prepare N-(11)C-met

288 ation, accumulation of total cholesterol and bile acids was prominently observed in the mutant liver,

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

290 y bile acids were similar, whereas secondary bile acids were absent, in GF mdr2(-/-) mice.

291 hanced Liver Fibrosis (ELF) scores and serum bile acids were also assessed.

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

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

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

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

296 Importantly, a panel of 20 bile acids were quantitatively measured, most of which h

297 ing genetic methods, the effects of bile and bile acids were shown to require the invasion gene trans

298 Primary bile acids were similar, whereas secondary bile acids we

299 tobiliary uptake and secretion of conjugated bile acids with PET and the (11)C-labeled conjugated bil

300 s critical for the functional interaction of bile acids with the channel.