ライフサイエンスコーパス: bile acid synthesis

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

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

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

4 three negative regulatory pathways controls bile acid synthesis.

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

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

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

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

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

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

11 tion of cholesterol absorption and repressed bile acid synthesis.

12 safely harnessing FGF19 biology to suppress bile acid synthesis.

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

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

15 hepatic cholestasis associated with impaired bile acid synthesis.

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

17 5beta-reductase is a key enzyme involved in bile acid synthesis.

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

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

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

21 in cholesterol levels through inhibition of bile acid synthesis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

56 Bile acid synthesis and pool size increases in diabetes,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 FGF19 inhibits bile acid synthesis in liver through transcriptional rep

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

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

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

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

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

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

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

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

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

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

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

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

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

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

122 Bile acid synthesis increased 70% in both genotypes.

123 The rate of bile acid synthesis influences colonic transit.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 Bile acid synthesis not only produces physiological dete

141 Bile acid synthesis occurs mainly via two pathways: the

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

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

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

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

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

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

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

149 Bile acid synthesis plays a critical role in the mainten

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

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

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

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

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

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

156 -33a may be a potential strategy to increase bile acid synthesis to maintain lipid homeostasis and pr

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

158 1H4 or farnesoid X receptor [FXR]) regulates bile acid synthesis, transport, and catabolism.

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

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

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

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

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

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

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

166 7alpha-hydroxylase, the limiting enzyme for bile acid synthesis, was elevated, unresponsive to dieta

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

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

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

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

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

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

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