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Primary bile acid biosynthesis - Reference pathway - …

T1 - Cholesterol binding to cytochrome P450 7A1, a key enzyme in bile acid biosynthesis

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Bile Acid Synthesis, Metabolism and Biological Functions

In animal models, this led to asignificant reduction of blood and body cholesterol and an increase in fecalsterol output, mostly neutral sterols.

A documented review on bile acids,present in all vertebrates except fish and bile alcohol present in fish, may beconsulted ().

Bile acids determination : As early as 1974, an almost completeseparation of bile acids was done by TLC ().

The most abundant bile acids in human bile are chenodeoxycholic acid (45%) and cholic acid (31%).

In mammals, the most common bile acids are C24 steroids with a carboxyl group atC-24 and up to three hydroxyl groups on the steroid nucleus, one being at C-3.

Bile Acid Synthesis and Utilization

REGULATION OF BILE ACID BIOSYNTHESIS - …

Within the liver the carboxyl group of primary and secondary bile acids is conjugated via an amide bond to either glycine or taurine before theirsecretion into the bile.

Within the intestines the primary bile acids areconverted by bacteria into the secondary bile acids, identified as deoxycholate (from cholate) and lithocholate (fromchenodeoxycholate).

Neutral pathway of bile acid biosynthesis (left)

Bile acid synthesis occurs in liver cells ..

AB - Background-The bioactive steroid, marinobufagenin, is an endogenous Na/K-ATPase bufadienolide inhibitor that is synthesized by adrenocortical and placental cells. Marinobufagenin binding to Na/K-ATPase initiates profibrotic cell signaling, and heightened marinobufagenin levels are implicated in the pathogenesis of hypertension, preeclampsia, and chronic kidney disease. Steroids are derived from cholesterol through the traditional steroidogenesis pathway initiated by enzyme CYP11A1, and via the acidic bile acid pathway, which is controlled by enzyme CYP27A1. The mechanism of marinobufagenin biosynthesis in mammals, however, remains unknown. Methods and Results-Here, we show that post-transcriptional silencing of the CYP27A1 gene in human trophoblast and rat adrenocortical cells reduced the expression of CYP27A1 mRNA by 70%, reduced total bile acids 2-fold, and marinobufagenin levels by 67% when compared with nontreated cells or cells transfected with nontargeting siRNA. In contrast, silencing of the CYP11A1 gene did not affect marinobufagenin production in either cell culture, but suppressed production of progesterone 2-fold in human trophoblast cells and of corticosterone by 90% in rat adrenocortical cells when compared with cells transfected with nontargeting siRNA. In vivo, in a high-salt administration experiment, male and female Dahl salt-sensitive rats became hypertensive after 4 weeks on a high-NaCl diet, their plasma marinobufagenin levels doubled, and adrenocortical CYP27A1 mRNA and protein increased 1.6-fold and 2.0-fold. Conclusions-Therefore, the endogenous steroidal Na/K-ATPase inhibitor, marinobufagenin, is synthesized in mammalian placenta and adrenal cortex from cholesterol through the novel acidic bile acid pathway. These findings will help to understand the role of marinobufagenin in highly prevalent human cardiovascular diseases.

The primary bile acids, cholic acid and chenodeoxycholic acid, are synthesized in the liver and conjugated with taurine or glycine before secretion via bile into the intestine.

Bile acid biosynthesis - Biochemistry (ACS Publications)
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  • Regulation of bile acid synthesis (PDF Download …

    Bile acid biosynthesis

  • 10/01/2018 · Regulation of bile acid synthesis

    Identification of intermediates in the bile acid synthetic pathway as ligands for the farnesoid X receptor

  • Regulation of Bile Acid Biosynthesis (PDF Download …

    PGC-1α Activates CYP7A1 and Bile Acid Biosynthesis

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pathway for bile acid biosynthesis

Background-The bioactive steroid, marinobufagenin, is an endogenous Na/K-ATPase bufadienolide inhibitor that is synthesized by adrenocortical and placental cells. Marinobufagenin binding to Na/K-ATPase initiates profibrotic cell signaling, and heightened marinobufagenin levels are implicated in the pathogenesis of hypertension, preeclampsia, and chronic kidney disease. Steroids are derived from cholesterol through the traditional steroidogenesis pathway initiated by enzyme CYP11A1, and via the acidic bile acid pathway, which is controlled by enzyme CYP27A1. The mechanism of marinobufagenin biosynthesis in mammals, however, remains unknown. Methods and Results-Here, we show that post-transcriptional silencing of the CYP27A1 gene in human trophoblast and rat adrenocortical cells reduced the expression of CYP27A1 mRNA by 70%, reduced total bile acids 2-fold, and marinobufagenin levels by 67% when compared with nontreated cells or cells transfected with nontargeting siRNA. In contrast, silencing of the CYP11A1 gene did not affect marinobufagenin production in either cell culture, but suppressed production of progesterone 2-fold in human trophoblast cells and of corticosterone by 90% in rat adrenocortical cells when compared with cells transfected with nontargeting siRNA. In vivo, in a high-salt administration experiment, male and female Dahl salt-sensitive rats became hypertensive after 4 weeks on a high-NaCl diet, their plasma marinobufagenin levels doubled, and adrenocortical CYP27A1 mRNA and protein increased 1.6-fold and 2.0-fold. Conclusions-Therefore, the endogenous steroidal Na/K-ATPase inhibitor, marinobufagenin, is synthesized in mammalian placenta and adrenal cortex from cholesterol through the novel acidic bile acid pathway. These findings will help to understand the role of marinobufagenin in highly prevalent human cardiovascular diseases.

Bile acids: regulation of synthesis

T1 - Synthesis of an Endogenous Steroidal Na Pump Inhibitor Marinobufagenin, Implicated in Human Cardiovascular Diseases, Is Initiated by CYP27A1 via Bile Acid Pathway

The endocrine pathway may be a physiological pathway for bile acid ..

Expression of the enzymes involved in bile acid synthesis is highly regulated by transcription factors to ensure their availability during changing metabolic conditions.

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