Functions of the liver !

Concept
Exam priority: medium

The liver processes what is absorbed, makes blood proteins, stores energy, clears toxins and produces bile.

Updated 2026-11-01

Also called: Hepatic physiology, Liver lobule

See it in 3D: Liver · Portal vein · Hepatic veins · Proper hepatic artery · Gallbladder · Common bile duct

Key points

Synthesis: albumin (half-life ≈20 days), factors II, VII, IX and X (vitamin K–dependent), fibrinogen, carrier proteins and angiotensinogen.
Factor VII has the shortest half-life (≈6 h): prothrombin time (INR) is the first thing to change in acute liver failure.
Metabolism: glycogen synthesis and breakdown, gluconeogenesis in fasting, VLDL and cholesterol synthesis, ketogenesis and the urea cycle.
Biotransformation: phase I (cytochrome P450) and phase II (glucuronidation, sulfation, glutathione) to make substances water-soluble.
Acinar zones: zone 1 (periportal) gets the most oxygen; zone 3 (centrilobular) has the most P450 and is the most sensitive to ischemia and acetaminophen.
Tests: ALT and AST reflect hepatocyte injury; alkaline phosphatase and GGT, cholestasis; albumin and INR, synthetic function.

What it is

The liver receives gut blood through the portal vein and mixes it with arterial blood in the sinusoids, where every hepatocyte touches plasma. From there it controls glucose in fasting and after meals, makes albumin and most clotting factors, turns ammonia into urea, transforms drugs and hormones for excretion and produces bile. Its large functional reserve explains why symptoms appear late.

Key facts

It stores glycogen, vitamins A, D and B12, iron (ferritin) and copper.
Kupffer cells (sinusoidal macrophages) clear bacteria and endotoxin arriving through the portal vein.
Stellate cells store vitamin A; when activated they produce the fibrosis of cirrhosis.
It inactivates hormones: estrogens, aldosterone, insulin and glucagon. In cirrhosis, excess estrogen causes gynecomastia, palmar erythema and spider angiomas.
It conjugates bilirubin with UGT1A1 and excretes it into bile.

Reference values (adult, vary by laboratory)

Parameter	Value	Note
Serum albumin	≈3.5–5.0 g/dL
Total bilirubin	≈0.3–1.2 mg/dL
ALT	≈7–55 U/L
INR	≈0.8–1.2	without anticoagulants

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

Clinical notes

Cirrhosis: less synthesis (low albumin → edema and ascites; high INR → bleeding), portal hypertension and ammonia-driven encephalopathy.
Excess acetaminophen depletes glutathione; the metabolite NAPQI damages zone 3.
Viral hepatitis (A, B, C, E) remains a relevant cause of liver injury in Colombia; alcohol and metabolic fatty liver are increasingly common.
Gilbert syndrome: reduced UGT1A1 activity → mildly raised indirect bilirubin with fasting or stress, with no liver damage.

Test yourself

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

Why does the INR change before albumin in acute liver failure?

Factor VII has a half-life of ≈6 h and falls within hours once the liver stops making it; albumin lasts ≈20 days in blood and takes weeks to drop.

Why is zone 3 of the hepatic acinus the most damaged in shock and in acetaminophen poisoning?

It receives the least-oxygenated blood at the end of the sinusoid and holds the most cytochrome P450 enzymes, which form the toxic metabolite NAPQI.

What explains gynecomastia and spider angiomas in cirrhosis?

The liver inactivates less estrogen and more androgen is converted to estrogen peripherally; the estrogen excess causes gynecomastia, palmar erythema and telangiectasias.

A pattern with very high alkaline phosphatase and GGT and a near-normal ALT suggests what?

A cholestatic pattern: obstruction or impairment of bile flow (stone, tumour, cholangitis or drugs) rather than hepatocyte necrosis.

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See it in 3D

The structures of Durgical's 3D anatomy where it happens.

In Biochemistry

← All of physiology

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); Anatomy, Abdomen and Pelvis: Liver (StatPearls (NCBI Bookshelf), 2024); Hepatic Cirrhosis (StatPearls (NCBI Bookshelf), 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 71). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.