ライフサイエンスコーパス: bile acid synthesis

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

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

3 ular metabolite of glucose, controls hepatic bile acid synthesis.

4 e initial step in cholesterol catabolism and bile acid synthesis.

5 specific activity but no change in rates of bile acid synthesis.

6 termining enzyme in the "classic" pathway of bile acid synthesis.

7 wer FGF19/15 and resultant increased hepatic bile acid synthesis.

8 three negative regulatory pathways controls bile acid synthesis.

9 ed but does not seem to be rate limiting for bile acid synthesis.

10 n StAR protein coincided with an increase in bile acid synthesis.

11 effect of CYP7B1 overexpression on rates of bile acid synthesis.

12 ansport protein, led to a 5-fold increase in bile acid synthesis.

13 s both the classic and alternate pathways of bile acid synthesis.

14 te-limiting enzyme in the classic pathway of bile acid synthesis.

15 tion of cholesterol absorption and repressed bile acid synthesis.

16 yme can participate in all known pathways of bile acid synthesis.

17 rohepatic circulation rather than in de novo bile acid synthesis.

18 hepatic cholestasis associated with impaired bile acid synthesis.

19 oxylase (Cyp7a), the rate-limiting enzyme in bile acid synthesis.

20 5beta-reductase is a key enzyme involved in bile acid synthesis.

21 ase enzyme, active in the acidic pathway for bile acid synthesis.

22 D3 are associated with defects in congenital bile acid synthesis.

23 ey regulators of triglyceride metabolism and bile acid synthesis.

24 ne biosynthesis and the alternate pathway of bile acid synthesis.

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

26 safely harnessing FGF19 biology to suppress bile acid synthesis.

27 hways including FGF19-mediated repression of bile acid synthesis.

28 oxylase CYP7A1 and other enzymes involved in bile acid synthesis.

29 in cholesterol levels through inhibition of bile acid synthesis.

30 decrease in expression of genes involved in bile acid synthesis.

31 f hepatic CYP7A1, thus promoting the de novo bile acid synthesis.

32 ne, including Fgf15, a negative regulator of bile acid synthesis.

33 ot play a role in postprandial regulation of bile acid synthesis.

34 and facilitate FGF19-mediated repression of bile acid synthesis.

35 ctors that induce CYP7A1 gene expression and bile acid synthesis.

36 udy, we investigated the nutrient effects on bile acid synthesis.

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

38 n of PGC-1alpha in hepatoma cells stimulates bile acid synthesis.

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

40 investigate the role of TGFbeta1 in hepatic bile acid synthesis.

41 A1 that encodes the rate-limiting enzyme for bile acid synthesis.

42 n 7alpha-hydroxylase expression and hence in bile acid synthesis.

43 n the p38 signaling pathway, HNF-4alpha, and bile acid synthesis.

44 reases in diabetes, whereas insulin inhibits bile acid synthesis.

45 Cholestyramine feeding stimulated bile acid synthesis 3.7 fold in both (-/-) and (+/+) mic

46 l 7-hydroxylase is a rate-limiting enzyme in bile acid synthesis, a major pathway for cholesterol cat

47 nt adaptive response; there was no change in bile acid synthesis, ABCG5/G8 expression, or hepatic cho

48 circulation of bile acids leads to increased bile acid synthesis and a reduction in plasma LDL-choles

49 tissues, reverse cholesterol transport, and bile acid synthesis and absorption.

50 s believed to be preferentially utilized for bile acid synthesis and biliary secretion.

51 reabsorption of bile acids, thus increasing bile acid synthesis and consequently cholesterol consump

52 ore, Pon3KO mice exhibited decreased hepatic bile acid synthesis and decreased bile acid levels in th

53 n may play a major role in the regulation of bile acid synthesis and dyslipidemia in diabetes.

54 o was predicted to exhibit reduced secondary bile acid synthesis and elevated aromatic amino acid cat

55 sis of the liver transcriptome revealed that bile acid synthesis and fibrosis gene expression levels

56 gene and suggests a discordant regulation of bile acid synthesis and gluconeogenesis by glucagon in h

57 hat may play a key role in the regulation of bile acid synthesis and gluconeogenesis in the liver.

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

59 pite compensatory changes in cholesterol and bile acid synthesis and in the expression of adenosine t

60 use livers suggesting enhanced repression of bile acid synthesis and increased efflux of bile acids i

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

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

63 the serum, which caused an increased hepatic bile acid synthesis and lipogeneses.

64 5 signaling and subsequently reduced hepatic bile acid synthesis and lipogenesis and attenuated ALD.

65 ase (CYP7A1) is tightly regulated to control bile acid synthesis and maintain lipid homeostasis.

66 t transactivator of the human CYP7A1 gene in bile acid synthesis and phosphoenolpyruvate carboxykinas

67 e clearly established a relationship between bile acid synthesis and plasma LDL-cholesterol concentra

68 ydroxylase activity is increased 5-fold, but bile acid synthesis and pool size are 47 and 27%, respec

69 Bile acid synthesis and pool size increases in diabetes,

70 ver FGF19/FGFR4 signaling pathway to inhibit bile acid synthesis and prevent accumulation of toxic bi

71 The JNK/c-Jun signaling pathway inhibits bile acid synthesis and protects hepatocytes against the

72 holate as an important negative regulator of bile acid synthesis and provide preliminary evidence for

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

74 iption of genes to allow feedback control of bile acid synthesis and secretion.

75 e studies confirm the importance of CYP27 in bile acid synthesis and they reveal an unexpected functi

76 decrease in mRNAs encoding genes controlling bile acid synthesis and transport as well as a variety o

77 eostasis by regulating genes responsible for bile acid synthesis and transport in humans, including c

78 of the B6By strain suggests a higher rate of bile acid synthesis and transport in these mice.

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

80 as genes involved in fatty acid trafficking, bile acid synthesis and uptake, and inflammatory respons

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

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

83 analyses revealed that pathways of secondary bile-acid synthesis and biotin metabolism were present,

84 ulating the expression of genes critical for bile-acid synthesis and hydrophobicity in the liver.

85 it with fasting serum 7alphaC4 (surrogate of bile acid synthesis) and FGF19 (negative regulator of bi

86 xylase, which is the rate-limiting enzyme in bile acid synthesis, and activated the gene encoding int

87 olic pathways: steroid hormone biosynthesis, bile acid synthesis, and conversion of lanosterol to cho

88 ylase (Cyp7a1), the rate-limiting enzyme for bile acid synthesis, and decreased plasma 7alpha-hydroxy

89 in gluconeogenesis, cholesterol homeostasis, bile acid synthesis, and proliferation in hepatocyte cel

90 humans and define a further inborn error in bile acid synthesis as a metabolic cause of severe chole

91 Bile acid synthesis (BAS) occurs mainly via two pathways

92 st, systemic FXR activation not only lowered bile acid synthesis but also suppressed proinflammatory

93 ificantly reduced capabilities for secondary bile acid synthesis but elevated capabilities for aromat

94 no significant effect on the rates of total bile acid synthesis but significantly increased (4.1-fol

95 CYP27 overexpression increased bile acid synthesis by <2-fold.

96 rol 27-hydroxylase (CYP27A1) is required for bile acid synthesis by both the classical and alternate

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

98 ow that the dietary vitamins A and D inhibit bile acid synthesis by repressing hepatic expression of

99 , Nr1h4) is a major mechanism in suppressing bile-acid synthesis by reducing the expression levels of

100 lternative pathway becomes a main pathway of bile acid synthesis capable of generating cholic and che

101 Inherited mutations that impair bile acid synthesis cause a spectrum of human disease; t

102 xhibited elevated cholesterol metabolism and bile acid synthesis coincident with unrepressed levels o

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

104 orter, ABC1, and the rate-limiting enzyme of bile acid synthesis, CYP7A1, respectively.

105 At 24 hours, bile acid synthesis decreased to 43% (P < 0.05) but retu

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

107 r pathways, such as lipoprotein assembly and bile acid synthesis, depend upon nCEH activity.

108 s hepatic cholesterol accumulation, impaired bile acid synthesis, disruption to glutamine/glutamate h

109 own the insulin receptor, FoxO1, and the key bile acid synthesis enzyme, CYP8B1.

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

111 d levels by modulating hepatic expression of bile acid synthesis enzymes, with a concomitant reductio

112 The rates of bile acid synthesis following a combination of StAR plus

113 A1) catalyses sterol side-chain oxidation of bile acid synthesis from cholesterol, and the first reac

114 retion, they express CYP7A1, which regulates bile acid synthesis from cholesterol.

115 ha-hydroxylase, the first enzyme involved in bile acid synthesis from cholesterol.

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

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

118 alpha) regulates genes involved in lipid and bile acid synthesis, gluconeogenesis, amino acid metabol

119 the down-regulation of key genes involved in bile acid synthesis, gluconeogenesis, and fatty acid bet

120 d hepatic dysfunction, a marked reduction of bile acid synthesis has been shown.

121 owth factor receptor 4 (FGFR4) in regulating bile acid synthesis has been well defined; however, its

122 -limiting enzyme in the classical pathway of bile acid synthesis, has been implicated in plasma chole

123 Linkage between bile acid synthesis, hepatocyte polarization, and regula

124 ocyte transport proteins and cholesterol and bile acid synthesis illustrated the development of chole

125 ur aim was to fully characterize a defect in bile acid synthesis in a 2-week-old African-American gir

126 iple study, by deleting a commensal gene for bile acid synthesis in a complex microbiome, we discover

127 sis genes resulted in a 3-fold lower rate of bile acid synthesis in a rat bile fistula animal model.

128 ylase and sterol 27-hydroxylase that control bile acid synthesis in classic and alternative pathways

129 ility of the hepatocyte to adapt its rate of bile acid synthesis in concert with the amount of choles

130 chanism underlying FGF15/FGF19 inhibition of bile acid synthesis in hepatocytes remains unclear.

131 molecular pathways responsible for reducing bile acid synthesis in hepatocytes, following treatment

132 inhibited the mRNA expression of CYP7A1 and bile acid synthesis in HepG2 cells and primary human hep

133 A1 and PEPCK mRNA expression and the rate of bile acid synthesis in HepG2 cells.

134 that HGF is a novel regulator of CYP7A1 and bile acid synthesis in human hepatocytes and may protect

135 FGF19 inhibits bile acid synthesis in liver through transcriptional rep

136 A decrease in bile acid synthesis in liver would reduce cholesterol ca

137 olesterol transport from peripheral tissues, bile acid synthesis in liver, and cholesterol absorption

138 cholesterol efflux in macrophages, promotes bile acid synthesis in liver, and inhibits intestinal ch

139 essed CYP7A1 mRNA expression and the rate of bile acid synthesis in primary human hepatocytes.

140 d specific transcriptional down-regulator of bile acid synthesis in primary rat hepatocytes, through

141 and butyrogenesis, and suppressed secondary bile acid synthesis in the African Americans.

142 This results in up-regulation of bile acid synthesis in the human hepatocytes and enlarge

143 paired in NCoA6(L2m/L2m) mice, which reduced bile acid synthesis in the liver and excretion in the fe

144 The TGFbeta1/Smad3 signaling may reduce bile acid synthesis in the liver and prevent hepatocyte

145 Bile acid synthesis in the liver is regulated by the rat

146 tion of HDL cholesterol ester catabolism and bile acid synthesis in the liver.

147 contributions of these two pathways to total bile acid synthesis in vivo.

148 F-4 transactivation of CYP7A1, a key gene in bile acid synthesis, in HepG2 cells, and mutation of the

149 -limiting enzyme in the alternate pathway of bile acid synthesis, in the liver of Syrian hamsters.

150 Bile acid synthesis increased 70% in both genotypes.

151 ed transcriptional signature for steroid and bile acid synthesis, indicating potential perturbation o

152 The rate of bile acid synthesis influences colonic transit.

153 w that 7alpha-hydroxylase and the pathway of bile acid synthesis initiated by this enzyme are essenti

154 The final step in bile acid synthesis involves conjugation with glycine an

155 We describe a metabolic defect in bile acid synthesis involving a deficiency in 7alpha-hyd

156 In older animals, an alternate pathway of bile acid synthesis involving an inducible oxysterol 7al

157 To understand if HIF-mediated decrease in bile acid synthesis is a physiologically relevant pathwa

158 Hepatic bile acid synthesis is controlled, in part, by a complex

159 lesterol 27-hydroxylase metabolic pathway of bile acid synthesis is expressed in neonatal life.

160 An "alternative" pathway of bile acid synthesis is initiated by sterol 27-hydroxylas

161 The rate of bile acid synthesis is reduced immediately after partial

162 Recent studies in mice suggest that bile acid synthesis is regulated by the fasted-to-fed cy

163 enzyme catalyzing the rate-limiting step of bile acid synthesis, is more sensitive to bile acid supp

164 termining enzyme in the alternate pathway of bile acid synthesis, is upregulated threefold in the PEX

165 synthesis) and FGF19 (negative regulator of bile acid synthesis) levels.

166 variation in negative feedback inhibition of bile acid synthesis may affect CDC-mediated acceleration

167 se, alternative mechanisms for regulation of bile acid synthesis may exist in human and hamster liver

168 Negative feedback regulation of bile acid synthesis mediated by the farnesoid X receptor

169 Bile acid synthesis not only produces physiological dete

170 acid metabolism is one such example wherein, bile acid synthesis occurs in the liver and its biotrans

171 Bile acid synthesis occurs mainly via two pathways: the

172 diated regulation of transcripts involved in bile acid synthesis or sterol efflux appear insensitive

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

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

175 lpha-hydroxylase, an enzyme of the alternate bile acid synthesis pathway with a sexually dimorphic ex

176 osterols and plays a role in the alternative bile acid synthesis pathway.

177 A1), the rate-limiting enzyme in the classic bile acid synthesis pathway.

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

179 Bile acid synthesis plays a critical role in the mainten

180 Bile acid synthesis plays a key role in regulating whole

181 tter feature ensures that the early phase of bile acid synthesis (pre-cholesterol) is in metabolic co

182 ated expression levels in B6By liver for key bile acid synthesis proteins, including cholesterol 7alp

183 acetaldehyde affects the enzyme activity and bile acid synthesis remains to be studied.

184 19/15-mediated hepatic repression of hepatic bile acid synthesis, resulting in hypercholanemia.

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

186 Despite increased bile acid synthesis, the bile acid pool size was decreas

187 aling defects, resulting in normalization of bile acid synthesis, the bile acid pool, and liver size.

188 egulating hepatic cholesterol catabolism and bile acid synthesis through the transcriptional control

189 -33a may be a potential strategy to increase bile acid synthesis to maintain lipid homeostasis and pr

190 wn-regulated the CYP7A1 and CYP8B1, shifting bile acid synthesis toward the acidic pathway to increas

191 1H4 or farnesoid X receptor [FXR]) regulates bile acid synthesis, transport, and catabolism.

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

193 The observed induction of bile acid synthesis via an alternative pathway or pathwa

194 conclusion, we show that seladelpar reduces bile acid synthesis via an FGF21-dependent mechanism tha

195 ex in the SHP-mediated inhibition of hepatic bile acid synthesis via coordinated chromatin modificati

196 t into mitochondria may be rate-limiting for bile acid synthesis via the "alternative" pathway.

197 is the predominant rate-determining step for bile acid synthesis via the alternative pathway.

198 On ursodiol therapy, hepatic bile acid synthesis was enhanced 2-fold compared with co

199 clear receptor SHP in feedback regulation of bile acid synthesis was examined.

200 7alpha-hydroxylase, the limiting enzyme for bile acid synthesis, was elevated, unresponsive to dieta

201 e major enzyme of the alternative pathway of bile acid synthesis, was not significantly different in

202 etic polymorphisms involved in regulation of bile acid synthesis were analyzed in the 36 patients wit

203 nd sterol 27-hydroxylase (S27H) and rates of bile acid synthesis were determined.

204 Similar changes in C7 alpha H, S27H, and bile acid synthesis were observed in primary rat hepatoc

205 expression of FGF19 , and key regulators of bile acid synthesis were related to KPE outcomes and liv

206 , and that there are alternative pathways of bile acid synthesis which begin with 27-hydroxylation of

207 ulated sterol 27-hydroxylase and alternative bile acid synthesis, which expanded the bile acid pool a

208 tion of hepatic LXR and Cyp7a1 led to higher bile acid synthesis, which may have contributed to incre