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Bile and the enterohepatic circulation !

  • Mechanism
  • Exam priority: high

The liver makes bile to emulsify fat; almost all bile salts are reabsorbed in the ileum and return to the liver to be used again.

Updated 2026-11-01

Also called: Bile salts, Enterohepatic cycle

See it in 3D: Liver · Gallbladder · Cystic duct · Common hepatic duct · Common bile duct · Ampulla of Vater · Ileum · Portal vein

What it is

Bile is the liver secretion that lets fat be digested and absorbed, and it is the exit route for cholesterol, bilirubin and many drugs. The gallbladder stores and concentrates it between meals, and CCK empties it into the duodenum. Bile salts are recycled: the terminal ileum reabsorbs ≈95% and the portal vein returns them to the liver several times a day (enterohepatic circulation).

How it works, step by step

  1. The hepatocyte converts cholesterol into primary bile acids and conjugates them with glycine or taurine.
  2. Canalicular pumps (BSEP) secrete them into bile with phospholipids, cholesterol and conjugated bilirubin; water follows by osmosis.
  3. Cholangiocytes, stimulated by secretin, add a bicarbonate-rich fluid (via CFTR and Cl⁻/HCO₃⁻ exchange).
  4. Between meals, the closed sphincter of Oddi diverts bile into the gallbladder, which absorbs Na⁺, Cl⁻ and water and concentrates it several-fold.
  5. Fat in the duodenum releases CCK: the gallbladder contracts and bile enters the duodenum through the ampulla of Vater.
  6. Above the critical micellar concentration, bile salts form micelles with fatty acids and monoglycerides and carry them to the brush border.
  7. In the terminal ileum ASBT reabsorbs bile salts; they travel in the portal vein and the hepatocyte takes them up efficiently (NTCP).
  8. Colonic bacteria deconjugate some and form secondary bile acids (deoxycholic, lithocholic); ileal FGF19 slows hepatic synthesis.

Approximate values (adult)

ParameterValueNote
Hepatic bile production≈0.6–1 L/day
Ileal reabsorption of bile salts≈95%per cycle
Enterohepatic cycles≈4–12 per daydepending on the number of meals
Concentration in the gallbladder≈5–10-foldup to ≈20 in some studies

Approximate values for a healthy adult at rest; each laboratory sets its own ranges.

Regulation

  • +CCK: Contracts the gallbladder and relaxes the sphincter of Oddi
  • +Secretin: Raises bicarbonate and water from the bile ducts
  • +Bile salts returning in the portal vein: The main stimulus for their own secretion (choleretic effect)
  • −FXR and ileal FGF19: Slow 7α-hydroxylase when many bile salts are returning

Clinical notes

  • Cholelithiasis: more common in women and with obesity, pregnancy, rapid weight loss and ileal disease (fewer bile salts).
  • Common bile duct obstruction: jaundice with high conjugated bilirubin, dark urine, pale stools and itching.
  • Conjugated bilirubin becomes urobilinogen in the colon; some is reabsorbed and excreted in urine (the enterohepatic cycle of bilirubin).
  • Bile acid–binding resins break the cycle: the liver takes up more LDL to make new bile acids.

Test yourself

Think of the answer, then tap the question to see it.

Why can terminal ileal resection cause steatorrhea even when the pancreas is normal?

Bile salts are reabsorbed there; if losses exceed the liver's ability to make new ones, the pool runs down, micelles fail and fat is not absorbed.

Which hormone contracts the gallbladder after a fatty meal, and what does it do to the sphincter of Oddi at the same time?

Cholecystokinin (CCK). It contracts the gallbladder and relaxes the sphincter of Oddi, so bile flows into the duodenum just when there is fat to emulsify.

Why does conjugating bile acids with glycine or taurine help fat digestion?

Conjugation lowers their pKa so they stay ionized at intestinal pH; they are not passively absorbed in the jejunum and remain in the lumen forming micelles until the ileum.

What property of bile favours cholesterol gallstones?

Supersaturation: more cholesterol than bile salts and lecithin can keep in solution, plus gallbladder stasis or hypomotility that allows nucleation.

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In Biochemistry

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 23.6 Accessory Organs in Digestion: The Liver, Pancreas, and Gallbladder (OpenStax (Rice University), 2022); 23.7 Chemical Digestion and Absorption: A Closer Look (OpenStax (Rice University), 2022); Gallstones (Cholelithiasis) (StatPearls (NCBI Bookshelf), 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 65). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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