Cholestrol
On this page 5 sections
| Lipoprotein | Highest Composition Component | Main Function |
| Chylomicron | Triglycerides (Dietary) | Transports dietary TGs to peripheral tissues |
| VLDL | Triglycerides (Endogenous) | Transports liver-synthesized TGs to peripheral tissues |
| LDL | Cholesterol | Delivers cholesterol to peripheral tissues |
| HDL | Protein | Scavenges cholesterol from tissues back to liver |
Major lipoproteins
| Lipoprotein | Main role | High-yield association |
|---|---|---|
| Chylomicrons | Transport dietary triglycerides from intestine | ApoB-48 |
| VLDL | Transport liver-derived triglycerides | ApoB-100 |
| IDL | Intermediate formed during VLDL metabolism | Can be taken up by liver or converted to LDL |
| LDL | Delivers cholesterol to peripheral tissues | Major atherogenic cholesterol carrier |
| HDL | Participates in reverse cholesterol transport | ApoA-I activates LCAT |
Apolipoproteins
| Apolipoprotein | Main function |
|---|---|
| ApoA-I | Activates LCAT; major HDL apoprotein |
| ApoB-48 | Required for chylomicron assembly |
| ApoB-100 | Structural protein of VLDL, IDL and LDL; binds LDL receptor |
| ApoC-II | Activates lipoprotein lipase (LPL) |
| ApoE | Mediates hepatic uptake of remnant particles |
Lipoprotein metabolism
Exogenous pathway
- Intestinal cells package dietary triglycerides and cholesterol into chylomicrons.
- Chylomicrons enter lymph and then blood.
- ApoC-II activates LPL, which hydrolyzes triglycerides.
- Fatty acids enter tissues.
- Chylomicron remnants, carrying ApoE, are taken up by the liver.
Endogenous pathway
- The liver secretes VLDL.
- LPL removes triglycerides, producing IDL.
- IDL is either taken up by the liver or further metabolized into LDL.
- LDL delivers cholesterol to tissues and is cleared through LDL receptors.
Reverse cholesterol transport
HDL accepts cholesterol from peripheral cells. LCAT esterifies cholesterol, helping retain it within HDL particles for transport toward the liver and other pathways of elimination.
Hyperlipoproteinemia Patterns
| Type | Main abnormality | Typical association |
|---|---|---|
| I | Chylomicrons increased | LPL or ApoC-II deficiency; severe hypertriglyceridemia |
| IIa | LDL increased | Familial hypercholesterolemia; premature atherosclerosis |
| IIb | LDL and VLDL increased | Combined hyperlipidemia |
| III | Remnant particles/IDL-like particles increased | ApoE-related remnant clearance defect; palmar xanthomas may occur |
| IV | VLDL increased | Hypertriglyceridemia, often associated with insulin resistance |
| V | Chylomicrons and VLDL increased | Severe hypertriglyceridemia; pancreatitis risk |
Clinical distinctions
- Type I: severe triglyceride elevation and pancreatitis risk; isolated chylomicron excess is not usually associated with accelerated atherosclerosis.
- Type IIa: LDL excess increases premature atherosclerosis risk.
- Type III: remnant accumulation; palmar crease xanthomas are a classic clue.
- Type IV: VLDL excess, often associated with obesity and diabetes.
- Type V: both chylomicrons and VLDL are elevated, with substantial pancreatitis risk if triglycerides are very high.