ライフサイエンスコーパス: bile acid

1 abolism (glucose), and liver function (total bile acids).

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

3 crucial for the enterohepatic circulation of bile acids.

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

5 chia, and Enterococcus and increased primary bile acids.

6 in mice with liver injuries and dysregulated bile acids.

7 bolites and enabled the detection of certain bile acids.

8 cholesterol, generating steroid hormones or bile acids.

9 ss people are associated with differences in bile acids.

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

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

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

13 ophobic interactions between polyphenols and bile acids.

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

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

16 o accommodate the amphipathic cholic core of bile acids, a fingerprint of key residues to recognize d

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

18 that, besides facilitating lipid absorption, bile acids act as signaling molecules that modulate gluc

19 Bile acids act on several receptors such as Farnesoid X

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

21 ation of the host innate immune response via bile acid-activated receptors FXR and TGR5 represents a

22 ecal and colonic inflammatory transcriptome, bile acid-activated receptors nuclear farnesoid X recept

23 ember of the nuclear receptor superfamily of bile acid-activated transcription factors and an importa

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

25 Alcohol purification showed that bile acid adsorption is independent of protein and fibre

26 insulin sensitivity, suggesting that raised bile acids affect beta-cell mass but are insufficient to

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

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

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

30 a well-known transcriptional corepressor of bile acid and lipid metabolism in the liver; however, it

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

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

33 ombinant mouse Nape-pld to screen a panel of bile acids and a library of experimental compounds (the

34 Serum bile acids and autotaxin activity remained unchanged.

35 nse during acute GvHD might be influenced by bile acids and by the decreased production of AhR ligand

36 both transport endogenous substrates such as bile acids and hormone conjugates as well as numerous dr

37 he relative abundance of cholic-acid-derived bile acids and induces physiologically relevant shifts i

38 el for bacterial enterotoxins and endotoxin, bile acids and interaction with the pharmaceutical drugs

39 oss-membrane signalling of a vast variety of bile acids and is a signalling hub in the liver-bile aci

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

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

42 in aryl hydrocarbon receptor (AhR) ligands, bile acids and plasmalogens.

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

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

45 Therefore, we propose that raised serum bile acids and reduced FXR and TGR5 activity contribute

46 key physiological pathways (e.g., involving bile acids and uric acid).

47 , alpha diversity, and pyrimidine, secondary bile acid, and neuroactive glucocorticoid/pregnanolone-t

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

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

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

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

52 olic homeostasis of lipids, glucose, energy, bile acids, and minerals.

53 ostridia), metabolite pools (acylcarnitines, bile acids, and short-chain fatty acids), and levels of

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

55 Bile acids are cholesterol metabolites that can signal t

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

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

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

59 Bile acids are recognized as signaling molecules regulat

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

61 proteins are secreted basolaterally, whereas bile acids are secreted apically.

62 Bile acids are synthesized from cholesterol in the liver

63 Bile acids are synthesized in the liver, stored in the g

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

65 levels were measured using the Diazyme Total Bile Acid Assay kit.

66 l therapeutic efficacy of CFTR inhibition in bile acid-associated diarrheas.

67 along the gut-liver axis acts as a sensor of bile acid availability to restrain liver size and tumori

68 onal cholesterol absorption, cholesterol and bile acid (BA) levels, and composition of BAs were measu

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

70 tirome (GC-1), are known to impact lipid and bile acid (BA) metabolism and induce hepatocyte prolifer

71 echanisms by which alterations in intestinal bile acid (BA) metabolism improve systemic glucose toler

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

73 The bile acid (BA) nuclear receptor, farnesoid X receptor (F

74 tholog FGF19) in the gut to potently inhibit bile acid (BA) synthesis in the liver.

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

76 clear receptors as key regulators of hepatic bile acid (BA)/lipid metabolism and inflammation.

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

78 Bile acids (BA), with their large hydrophobic steroid nu

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

80 Bile acids (BAs) are diverse molecules that are synthesi

81 Bile acids (BAs) are important regulators of metabolism

82 Bile acids (BAs) are key mediators of the glycemic contr

83 Bile acids (BAs) are known facilitators of nutrient abso

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

85 Bile acids (BAs) comprise heterogenous amphipathic chole

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

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

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

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

90 lated in cholestatic patient sera, including bile acids (BAs).

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

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

93 h intrahepatic cholestasis of pregnancy have bile acids below this concentration, they can probably b

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

95 s in the orthosteric site, a putative second bile acid-binding site with allosteric properties and st

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

97 found that, depending on the bile acid used, bile acids both activate and inhibit mouse ENaC.

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

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

100 Bile acid composition and leucine fermentation defined a

101 utrient content in the gut, which influences bile acid composition and pool size.

102 ith changes in the microbiota population and bile acid composition, including reversing microbiota co

103 at least 30 participants, and that reported bile acid concentrations and perinatal outcomes.

104 lipolysis and lipotoxic injury, CEL required bile acid concentrations higher than in human fat necros

105 ahepatic cholestasis of pregnancy when serum bile acid concentrations were available.

106 sed by maternal pruritus and increased serum bile acid concentrations, is associated with increased r

107 egnancy and singleton pregnancies when serum bile acids concentrations are of 100 mumol/L or more.

108 These bile-acid conjugates were also found in humans, and were

109 Cecal bile acid conjugation was reduced in pregnancy because o

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

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

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

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

114 d intestinal microbiota of pregnancy enhance bile acid deconjugation, reducing ileal bile acid uptake

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

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

117 e microbial metabolic byproduct of secondary bile acid deoxycholic acid (DCA), at as low as 50 uM, in

118 ns, or its derived metabolite, the secondary bile acid deoxycholic acid, can restore pDC- and MyD88-d

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

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

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

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

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

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

125 Bile acid diarrhea (BAD) is common with ileal resection,

126 erologic tests for celiac disease, tests for bile acid diarrhea, the commercially available version o

127 chloride secretion as potential therapy for bile acid diarrhea.

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

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

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

131 salt hydrolase activity, which deconjugates bile acids enabling secondary modification to FXR agonis

132 Bile acids facilitate nutrient absorption and are endoge

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

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

135 uced Cyp7a1 in DKO mice, suggesting impaired bile acid feedback regulation.

136 e screened the major species of deconjugated bile acids for their ability to potentiate the different

137 we inferred elevated production of secondary bile acids from CRC metagenomes, suggesting a metabolic

138 alterations could be overcome by intestinal bile acids functioning as FXR agonists.

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

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

141 imed to investigate the role of raised serum bile acids, FXR and TGR5 in gestational glucose metaboli

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

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

144 Potential mechanisms include disruption of bile acid homeostasis and reduction in the production of

145 Furthermore, restoring bile acid homeostasis by farnesoid X receptor activation

146 axis that regulates hepatic cholesterol and bile acid homeostasis.

147 The G6P-ChREBP-dependent change in bile acid hydrophobicity associates with elevated plasma

148 as a major prosecretory mechanism of CDCA, a bile acid implicated in BAD, and support the potential t

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

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

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

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

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

154 hich was correlated with changes observed in bile acids in exposed birds.

155 d phenolic compounds in urine (UHPLC-MS/MS), bile acids in feces (UHPLC-QTOF), gastrointestinal condi

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

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

158 es studying the role of elevated circulating bile acids in metabolic control.

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

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

161 d the overall intracellular concentration of bile acids in primary human hepatocytes grown in sandwic

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

163 conditions characterized by accumulation of bile acids in the liver that actively contribute to live

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

165 erprint of key residues to recognize diverse bile acids in the orthosteric site, a putative second bi

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

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

168 Factor-15/19 (mouse FGF15, human FGF19) are bile acid-induced late fed-state gut hormones that decre

169 ted that endotoxin sensitizes hepatocytes to bile-acid-induced cell death.

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

171 mproved CCS calibration for phospholipid and bile acid isomers.

172 Lithocholic bile acid (LCA) has been reported to selectively kill ca

173 We find that serum total bile acid levels directly correlate with the PTB rates r

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

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

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

177 Bile acid malabsorption (BAM) and bile acid-related diar

178 Bile acid malabsorption (BAM) was identified in patients

179 to a combination of the effects of increased bile acids, maternal dyslipidemia and deranged maternal

180 In contrast, Mst1/2 deficiency impairs bile acid metabolism and remarkably increases Cyp7a1 exp

181 These findings identify dysregulated bile acid metabolism as a potential therapeutic target i

182 neurotensin (NT)] and on glucose, lipid, and bile acid metabolism in RYGB-operated and unoperated ind

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

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

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

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

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

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

189 ddition, metabolites associated with hepatic bile acid metabolism were affected by oil exposure which

190 factors, including a defective gut barrier, bile acid metabolism, antibiotic use, and the pleiotropi

191 Bile acid metabolism, in turn, is controlled by several

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

193 FGF15 activates Hippo signaling to suppress bile acid metabolism, liver overgrowth, and tumorigenesi

194 rylation, fatty acid metabolism, peroxisome, bile acid metabolism, xenobiotic metabolism, and adipoge

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

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

197 -sensitive aromatic amino acid and secondary bile acid metabolism.

198 ed expression of genes involved in lipid and bile acid metabolism.

199 te of glucose, glucose-6-phosphate (G6P), on bile acid metabolism.

200 cid (BAA485), a potential microbiome-derived bile acid metabolite.

201 g, we identified lower levels of circulating bile acid metabolites in multiple cohorts of adult and p

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

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

204 integrated analysis of gut microbiome, serum bile acid metabolome, imaging, and histological measurem

205 e acids and is a signalling hub in the liver-bile acid-microbiota-metabolism axis(1-3).

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

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

208 on the position and orientation of specific bile acid moieties.

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

210 y lupin compounds that interact with primary bile acids on molecular level.

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

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

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

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

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

216 1 mRNA and protein in DKO mice and increased bile acid pool size, while cholic acid also induced Cyp7

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

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

219 red that lithocholic acid (LCA), a secondary bile acid prevalent in the cecum and colon of mice and h

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

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

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

223 d remarkably increases Cyp7a1 expression and bile acid production.

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

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

226 The G-protein-coupled bile acid receptor (GPBAR) conveys the cross-membrane si

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

228 ase through its effects on G protein-coupled bile acid receptor 1 (GPBAR1).

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

230 Global G protein-coupled bile acid receptor-1 null (Tgr5(-/-)) and intestinal-spe

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

232 gate the role of the gut microbiome and TGR5 bile acid receptors in MDMA-mediated hyperthermia.

233 bolic effects of the deficiency of these two bile acid receptors on hepatic metabolism and injury in

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

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

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

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

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

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

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

241 Bile acid malabsorption (BAM) and bile acid-related diarrhea represent an under-recognized

242 The high bile acid requirements for effective lipolysis make CEL

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

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

245 ent and principally in vitro cholesterol and bile acid/salts binding ability.

246 hocholic acid (P = 0.01) and total secondary bile acid (SBA) concentrations (P = 0.04) than the oleic

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

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

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

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

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

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

253 -1 receptor antagonist, or cholestyramine, a bile acid sequestrant.

254 Bile acid sequestrants are orally administered polymers

255 Bile acid sequestrants interrupt intestinal reabsorption

256 d, we were able to identify dysregulation of bile acids, short-chain fatty acids, and cholesterol der

257 in and streptomycin markedly altered hepatic bile acid signaling and lipid metabolism, while ceftriax

258 of a variety of endogenous compounds such as bile acids, steroids, and fat-soluble vitamins, as well

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

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

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

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

263 Bile acid synthesis plays a key role in regulating whole

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

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

266 reased levels of LDH as well as reduction in bile acid synthesis-results that were consistent with he

267 report a role of TFEB in regulating hepatic bile acid synthesis.

268 in type 2 diabetes associates with perturbed bile acid synthesis.

269 s enzyme Cyp7a1 expression, thereby limiting bile acid synthesis.

270 h the compounds showed reduced expression of bile-acid synthesis genes in vivo.

271 s and stabilizes SHP to downregulate the key bile acid-synthesis enzyme Cyp7a1 expression, thereby li

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

273 n in the general population, provided repeat bile acid testing is done until delivery.

274 metalloproteinase 1, C-reactive protein, and bile acids than nonresponders.

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

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

277 tified a series of noncanonical, unsaturated bile acids that were depleted in patients with CDI.

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

279 (ICP) causes increased transfer of maternal bile acids to the fetus and an increased incidence of su

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

281 fetus in ICP by inhibiting OATP4A1-mediated bile acid transfer and TC-induced placental vasoconstric

282 metabolism, basic amino acid metabolism, and bile acid transport.

283 estinal bile acid uptake by an apical sodium-bile acid transporter (ASBT) inhibitor decreases ileal F

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

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

286 Therefore, bile acid transporter-mediated oral drug delivery has be

287 iated by interactions with the apical sodium bile acid transporter.

288 As mithramycin affects cellular response to bile acid treatment by altering the expression of multip

289 n paid to short-chain fatty acids, secondary bile acids, trimethylamine N-oxide, and phenylacetylglut

290 ance bile acid deconjugation, reducing ileal bile acid uptake and lowering FXR induction in enterocyt

291 Consistently, blocking intestinal bile acid uptake by an apical sodium-bile acid transport

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

293 Administration of the secondary bile acid ursodeoxycholic acid (UDCA; ursodiol) inhibits

294 study ENaC, we found that, depending on the bile acid used, bile acids both activate and inhibit mou

295 ostridium scindens strain produces secondary bile acids via dehydroxylation.

296 Whether bile acids were activating or inhibiting was contingent

297 singly negatively charged phospholipids and bile acids were calibrated in nitrogen buffer gas using

298 erum C4 compared with placebo; reductions in bile acids were greatest with 100 mg.

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

300 th a 1,000-fold reduction in serum secondary bile acids, which was highly correlated with AP-1/NR4A s