Structure of a lipoprotein particle
Each transport particle has a specialized structure adapted for circulation in the aqueous blood environment:
- Hydrophobic core: the central part containing cholesterol esters and triglycerides.
- Shell (surface layer): the less hydrophobic contact zone with blood, consisting of free cholesterol and phospholipids.
- Apolipoproteins: protein components on the surface that serve as ligands for cellular receptors and activate enzymes.
Classification and functions of classes
The blood lipid profile is represented by several classes of particles:
- Chylomicrons (CMs): formed in enterocytes from dietary fats, containing up to 95% triglycerides. Markers are Apo B-48 and Apo C.
- VLDLs: transport endogenous triglycerides, contain Apo B-100 and Apo E, and exhibit atherogenic activity.
- IDLs: a transitional and unstable form with an equal ratio of cholesterol and triglycerides, rapidly converting into LDLs.
- LDLs: the main carriers of cholesterol to the periphery (up to 55%), the key atherogenic fraction.
- HDLs: rich in phospholipids and proteins, responsible for reverse cholesterol transport to the liver.
Metabolism and enzymatic cleavage
The transformation of particles in the bloodstream is associated with the action of enzymes and receptors:
- In tissue capillaries, triglycerides of chylomicrons and VLDLs are cleaved by endothelial lipoprotein lipase.
- The key activator of this lipase is Apo C located on the particle surface.
- As a result of lipolysis, chylomicrons turn into remnants, while VLDLs transform into IDLs and further into LDLs.
- The uptake of remnant particles by the liver occurs via receptor-mediated endocytosis.
Atherogenic and antiatherogenic components
The role of lipoproteins in vascular pathology is divided into two directions:
- Atherogenic component: all classes containing Apo B-100 (VLDLs, IDLs, LDLs) transport cholesterol from the liver to tissues and are capable of depositing in the vessel wall.
- Antiatherogenic component: HDLs do not contain Apo B-100, take excess cholesterol from tissues and deliver it to the liver for utilization, protecting blood vessels.
Briefly: answers to topical questions
How do hepatocytes take up chylomicron remnants?
The uptake of chylomicron remnants by the liver is carried out by hepatocytes via receptor-mediated endocytosis. Particle binding occurs with the participation of scavenger receptors and receptors for Apo B and E, after which chylomicron remnants are degraded in the lysosomes of liver cells.
The Apo B rule: particles with Apo B-100 go from the liver to the periphery and cause atherosclerosis (VLDLs, IDLs, LDLs), whereas HDLs without this protein clean the vessels.
Class and exam questions
Which lipoproteins transport exogenous lipids?
Exogenous (dietary) lipids are transported by chylomicrons, which are synthesized in the intestinal enterocytes.
Why are LDLs called an atherogenic fraction?
LDLs contain the maximum amount of cholesterol and the Apo B-100 protein, through which they deliver cholesterol to peripheral tissues via receptor-mediated endocytosis.
What function do HDLs perform?
HDLs perform reverse cholesterol transport, removing its excess from peripheral tissues and delivering it to the liver, making them the main antiatherogenic factor.
Which enzyme hydrolyzes triglycerides within chylomicrons and VLDLs?
Hydrolysis of triglycerides in tissue capillaries is carried out by endothelial lipoprotein lipase, activated by apolipoprotein C.
What else to study on this topic
- The role of hepatocyte scavenger receptors in the utilization of chylomicron remnants
- Synthesis of bile acids from cholesterol in the liver
- Molecular mechanisms of receptor-mediated LDL endocytosis
- Participation of lecithin-cholesterol acyltransferase in HDL metabolism
- Pathophysiology of cholesterol ester accumulation in the vessel wall
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