Biochemistry · Topic
Lipoprotein metabolism !
Lipoproteins carry fat in the blood: the exogenous pathway delivers dietary fat, the endogenous pathway liver fat, and HDL returns cholesterol to the liver.
Updated 2026-11-01
Key facts
- Exogenous: the gut builds chylomicrons (ApoB-48); LPL removes their triglyceride and the liver takes up remnants via ApoE.
- Endogenous: the liver secretes VLDL (ApoB-100); LPL turns it into IDL and then LDL, which the LDL receptor clears.
- Reverse transport: HDL picks up tissue cholesterol via ABCA1, LCAT esterifies it, and it reaches the liver via SR-BI or, through CETP, in ApoB particles.
- Key apos: B-48 (chylomicron), B-100 (VLDL/LDL, binds the receptor), C-II (activates LPL), E (remnant uptake), A-I (HDL, activates LCAT).
In detail
- In the enterocyte, MTP loads triglyceride, cholesterol and phospholipid onto ApoB-48: the chylomicron is born and leaves through the lymph (thoracic duct), bypassing the liver.
- In blood, HDL gives it ApoC-II and ApoE. In muscle and fat capillaries, LPL (activated by ApoC-II) releases the fatty acids.
- The shrunken chylomicron returns ApoC-II to HDL and becomes a cholesterol-rich remnant that the liver takes up via ApoE.
- The liver packs triglyceride made from surplus carbohydrate into VLDL with ApoB-100; LPL empties it, leaving IDL.
- Some IDL returns to the liver via ApoE; the rest loses more triglyceride to hepatic lipase and becomes cholesteryl-ester-rich LDL.
- LDL delivers cholesterol to tissues and liver via the LDL receptor; if it lingers in blood, it is oxidised in the artery wall and taken up by macrophages (foam cells).
- Nascent HDL (lipid-poor ApoA-I) takes cholesterol and phospholipid from cells via ABCA1; LCAT esterifies it and the particle becomes spherical.
- HDL hands cholesteryl ester to the liver via SR-BI, or CETP passes it to VLDL and LDL for triglyceride; the liver excretes it in bile.
Clinical notes
- A lipid panel measures total cholesterol, HDL and triglycerides; LDL is usually calculated (Friedewald), unreliable when triglycerides are very high.
- Fredrickson classes: I (chylomicrons), IIa (LDL), IIb (LDL and VLDL), III (remnants), IV (VLDL), V (VLDL and chylomicrons).
- Statins, ezetimibe and PCSK9 inhibitors lower LDL; fibrates activate PPAR-α and raise LPL activity.
Related conditions
- Atherosclerosis and dyslipidaemia
- Familial hypercholesterolemia
- Familial chylomicronemia syndrome (lipoprotein lipase deficiency)
- Abetalipoproteinemia (Bassen–Kornzweig syndrome)
- Familial dysbetalipoproteinemia (type III hyperlipoproteinemia)
- Tangier disease
- Acute pancreatitis
Related
- Chylomicron
- VLDL (very-low-density lipoprotein)
- LDL (low-density lipoprotein)
- HDL (high-density lipoprotein)
- Lipoprotein lipase (LPL)
- LCAT (lecithin–cholesterol acyltransferase)
- CETP (cholesteryl ester transfer protein)
- LDL receptor
- PCSK9
- Apolipoprotein B (ApoB-100 and ApoB-48)
- Apolipoprotein E (ApoE)
- Cholesterol
- Bile acid synthesis
- Cholesterol synthesis (mevalonate pathway)
Test yourself
Think of the answer, then tap the question to see it.
Which apolipoprotein defines the chylomicron, and which LDL?
ApoB-48 on chylomicrons; ApoB-100 on VLDL, IDL and LDL.
Why do chylomicrons reach the blood without passing through the liver?
They are too large for gut capillaries: they travel through lymphatics and the thoracic duct.
Which steps make up reverse cholesterol transport?
Efflux through ABCA1 to ApoA-I, esterification by LCAT and delivery to the liver (SR-BI or via CETP), which sends it to bile.
Which Fredrickson type is remnant accumulation?
Type III (dysbetalipoproteinaemia).
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Plasma lipoprotein assembly, remodeling, and clearance (R-HSA-174824) (Reactome, 2026); Cholesterol | High Cholesterol | MedlinePlus (MedlinePlus, US National Library of Medicine, 2026); Triglycerides | MedlinePlus (MedlinePlus, US National Library of Medicine, 2026); Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011).
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Representative model, for educational purposes only.