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Bile acids: the pathway in the body · Biomarker & Stool Analysis

This page shows the biochemical pathway behind the laboratory value Bile acids (stool): which stations follow one another, which enzymes carry out each step and which cofactors they use. Every statement has a source. The page describes general textbook knowledge and says nothing about any individual person.

In brief

Bile acids are derivatives of cholesterol that the liver forms and releases into the gut with the bile. There they surround fat droplets; gut bacteria modify them before part of them appears in stool. When many return, the liver slows new formation.

12 stations · 6 sources
ORYIn the liverIn the gutASBTSodiumCYP7A1NADPHOxygenCYP8B1, CYP27A1NADPHBAATGlycineTaurineBSEPATPFXRBile salt hydrolase7α-dehydroxylation7α-dehydroxylationwith bile into the gutColestyramineCholesterolstarting material7α-Hydroxycholesterolfirst stepCholic acid, CDCAprimary bile acidsConjugated bile acidwith glycine or taurineBileBSEP pumpBile acids in the gutcoat fat dropletsReuptake in the ileumASBT transporterFXR and FGF19feedback to the liverFree bile acidsglycine/taurine removedDeoxycholic acidsecondary bile acidLithocholic acidsecondary bile acidIn the stoolend of the pathway

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The pathway step by step

Each station states what the compound does there. Three signs: ↑ supplies — builds up or makes available · ↓ depletes — inhibits, consumes or withholds · ↕ both, depending on amount. Behind it stands what the statement rests on: established physiology, observed in studies, or contested. The signs do not grade; they name the direction.

  1. Cholesterol → 7α-Hydroxycholesterol CYP7A1 · NADPH, Oxygen The enzyme CYP7A1 attaches an OH group at position 7 of the ring. This is the slowest step of the whole pathway; here the liver regulates the amount formed. FXR and FGF19 slow it when many bile acids return. Source 1↑ supplies At this step the liver decides how much cholesterol goes into bile acids: if many bile acids return, FXR and FGF19 dampen the enzyme; if few return, more of it is made. established physiology Source 1, 5
    ⚖ When the balance tips

    too much — If CYP7A1 is very active, more cholesterol is converted into bile acids; this draws cholesterol out of the liver cell.

    too little — If CYP7A1 is strongly dampened, fewer bile acids form, and more cholesterol remains in the liver cell.

    established physiology · Source 1

  2. 7α-Hydroxycholesterol → Cholic acid, CDCA CYP8B1, CYP27A1 · NADPH Several further steps yield the two primary bile acids: cholic acid and chenodeoxycholic acid. The enzyme CYP8B1 decides which of the two is formed. Chenodeoxycholic acid reports the fill level via FXR. Source 1↑ supplies Cholic acid and chenodeoxycholic acid are the two basic forms. Chenodeoxycholic acid binds particularly strongly to the switch FXR and so reports how full the bile acid pool is. established physiology Source 5, 1
    ⚖ When the balance tips

    too much — If many primary bile acids accumulate in the liver cell, they activate FXR there too; this dampens CYP7A1 and CYP8B1 and increases release into the bile.

    too little — If few primary bile acids form, FXR remains little occupied, and the liver releases the brake on CYP7A1.

    established physiology · Source 5, 1

  3. Cholic acid, CDCA → Conjugated bile acid BAAT · Glycine, Taurine The enzyme BAAT attaches glycine or taurine. The bile acid thus stays dissolved even in acidic gut contents and is not simply absorbed through the gut wall. In this way it reaches the end of the small intestine. Source 1, 2↑ supplies Conjugation turns bile acids into well-dissolved salts. They stay in the gut until the end of the small intestine and are retrieved there specifically via ASBT instead of crossing the gut wall on the way. established physiology Source 2, 3
    ⚖ When the balance tips

    too much — If plenty of glycine and taurine is present, almost all bile acids are conjugated; more conjugation partners do not raise the amount of bile acids, because CYP7A1 sets it.

    too little — If little taurine is available, BAAT conjugates the bile acids increasingly with glycine; the ratio of the two forms shifts.

    established physiology · Source 1, 2

  4. Conjugated bile acid → Bile BSEP · ATP The BSEP pump moves bile acids out of the liver cell into the bile ducts, using ATP. From there they reach the small intestine via the gallbladder. The pumped bile acids drive bile flow. Source 3↑ supplies BSEP drives bile flow: the pumped bile acids draw water and other substances into the bile ducts after them. Between meals the gallbladder collects the bile. established physiology Source 2, 3
    ⚖ When the balance tips

    too much — If BSEP pumps many bile acids, more bile flows; reuptake in the ileum brings most of them back to the liver.

    too little — If BSEP works more slowly, bile acids build up in the liver cell and less bile reaches the gut; FXR in the liver cell then dampens new formation.

    established physiology · Source 3, 5

  5. Bile acids in the gut → Reuptake in the ileum ASBT · Sodium At the end of the small intestine, the ASBT transporter retrieves most of the bile acids. They return to the liver via the portal vein; this circuit is called enterohepatic. The same pool thus cycles several times a day. Source 3↑ supplies Reuptake keeps the bile acid pool in circulation: the same pool cycles several times a day between liver and gut, and only a small part has to be newly made. established physiology Source 3
    ⚖ When the balance tips

    too much — If ASBT retrieves many bile acids, more feedback reaches the liver via FXR and FGF19, and it makes fewer new ones.

    too little — If ASBT retrieves little, for example when colestyramine binds bile acids, more are lost with the stool; the liver then makes more from cholesterol.

    established physiology · Source 3, 5, 6

  6. Reuptake in the ileum → FXR and FGF19 FXR In the gut cell, bile acids bind to the switch FXR. The cell then forms FGF19, which travels through the blood to the liver and dampens the formation of CYP7A1 there. In this way the liver adjusts new formation. Source 5, 3↓ depletes FGF19 slows the new formation of bile acids in the liver; FXR in the gut cell also controls onward transport into the blood. New formation thus adapts to the returning amount. established physiology Source 5, 3
    ⚖ When the balance tips

    too much — If FXR is strongly activated, a lot of FGF19 is formed and the liver dampens CYP7A1 considerably; fewer new bile acids form.

    too little — If little FGF19 reaches the liver, for example because little returns, the brake falls away and the liver makes more bile acids from cholesterol.

    established physiology · Source 5

  7. Bile acids in the gut → Free bile acids Bile salt hydrolase Many gut bacteria carry the enzyme bile salt hydrolase (BSH). It splits off glycine or taurine, leaving the free bile acid. Only then can bacteria modify them further. Source 4↑ supplies Only after removal can bacteria modify bile acids further; they use taurine as a nutrient. Free bile acids partly pass back passively through the gut wall. established physiology Source 4, 3
    ⚖ When the balance tips

    too much — If bacteria remove a lot, more free bile acids form; they dissolve less well, contribute less to micelles, and more material is available for secondary bile acids.

    too little — If bacteria remove little, for example when their numbers in the gut fall, more bile acids stay conjugated and fewer secondary bile acids form.

    established physiology · Source 4, 2

  8. Free bile acids → Deoxycholic acid 7α-dehydroxylation A few bacterial species in the colon then remove the OH group at position 7. This turns cholic acid into deoxycholic acid. It is more fat-soluble than cholic acid. Source 4↕ both, depending on amount Deoxycholic acid is partly absorbed in the colon and then circulates with the other bile acids. It is more fat-soluble than cholic acid and in larger amounts acts like a detergent on cell membranes. observed in studies Source 4
    ⚖ When the balance tips

    too much — If a lot of deoxycholic acid accumulates, in cell culture and animal models it dissolves fats out of the membranes of gut cells and puts strain on the cells.

    too little — If little deoxycholic acid forms, for example when few bacteria carry out 7α-dehydroxylation, more cholic acid remains unchanged in the gut.

    observed in studies · Source 4

  9. Free bile acids → Lithocholic acid 7α-dehydroxylation By the same route, chenodeoxycholic acid becomes lithocholic acid. It dissolves poorly in water and therefore largely stays in the gut. What returns, the liver couples with sulphate. Source 4↓ depletes Lithocholic acid is the least soluble bile acid. In cell culture and animal models it puts strain on liver and gut cells in larger amounts; what returns, the liver couples with sulphate and excretes it that way. observed in studies Source 4
    ⚖ When the balance tips

    too much — If lithocholic acid builds up, for example when little of it is coupled with sulphate, in animal models it puts strain on the liver cells and slows bile flow.

    too little — If little lithocholic acid forms, more chenodeoxycholic acid remains unchanged in the gut.

    observed in studies · Source 4

  10. Deoxycholic acid → In the stool Whatever does not return to the blood leaves the body with the stool. This is why stool mainly contains the secondary bile acids remodelled by bacteria. What is lost here, the liver makes again from cholesterol. Source 4, 2↓ depletes Loss with the stool is the exit of the cycle: what is lost here, the liver makes again from cholesterol. In this way the total bile acid pool stays the same. established physiology Source 3, 1
    ⚖ When the balance tips

    too much — If many bile acids are lost with the stool, for example through colestyramine, the liver converts more cholesterol into bile acids; if new formation cannot keep up, the pool shrinks.

    too little — If few bile acids are lost, almost the whole pool returns to the liver, and it makes correspondingly few new ones.

    established physiology · Source 6, 3

  11. Lithocholic acid → In the stool Whatever does not return to the blood leaves the body with the stool. This is why stool mainly contains the secondary bile acids remodelled by bacteria. What is lost here, the liver makes again from cholesterol. Source 4, 2↓ depletes Loss with the stool is the exit of the cycle: what is lost here, the liver makes again from cholesterol. In this way the total bile acid pool stays the same. established physiology Source 3, 1
    ⚖ When the balance tips

    too much — If many bile acids are lost with the stool, for example through colestyramine, the liver converts more cholesterol into bile acids; if new formation cannot keep up, the pool shrinks.

    too little — If few bile acids are lost, almost the whole pool returns to the liver, and it makes correspondingly few new ones.

    established physiology · Source 6, 3

Further stations

Cofactors in this pathway

What acts on this pathway

Sources

  1. Chiang JY. Bile acids: regulation of synthesis. J Lipid Res 2009 · PubMed 19346330
  2. Di Ciaula A, Garruti G et al. Bile Acid Physiology. Ann Hepatol 2017 · PubMed 29080336
  3. Dawson PA, Karpen SJ. Intestinal transport and metabolism of bile acids. J Lipid Res 2015 · PubMed 25210150
  4. Ridlon JM, Kang DJ et al. Bile salt biotransformations by human intestinal bacteria. J Lipid Res 2006 · PubMed 16299351
  5. Chiang JYL, Ferrell JM. Discovery of farnesoid X receptor and its role in bile acid metabolism. Mol Cell Endocrinol 2022 · PubMed 35283218
  6. US prescribing information Colestyramine (DailyMed), section Clinical Pharmacology · Prescribing information

Related pathways

As of 2026-09-16. Draft, written by Claude to schema v2; sources checked in PubMed; expert approval pending
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