Cholesterol is created by the body's cells and absorbed from the diet. The liver processes absorbed cholesterol and is also responsible for about 25% of that manufactured by the body. Once created or intercepted, the liver prepares cholesterol and triglyceride for transport to the myriad of needy tissues throughout the body. Cholesterol is a lipid and does not mix easily with the watery environment of blood so it must be packaged in an appropriate way so to avoid it sticking to the sides of blood vessels. This is achieved by combining it with phospholipid, triglyceride, and a single large protein called apolipoprotein B100 (ApoB100). These packages are known as low density lipoproteins (LDL) and referred to as “bad cholesterol” in the clinical arena.
The LDL Receptor
Cells create small receptors (LDL receptors) specific for the uptake of cholesterol and insert these on the cell's surface or remove them as required. These receptors are specific for the attachment of ApoB100. When ApoB100 connects with the LDL receptor of a cell it triggers a complex mechanism leading to the intake of the entire LDL molecule. Once endocytosed (eaten), LDL cholesterol particles are processed by enzymes and used as substrates for membranes, hormones, and other products.
Atherosclerosis and LDL-Cholesterol
LDL cholesterol has achieved a negative reputation due to its association with atherosclerosis. This is a condition where the arteries thicken and gum up with plaques, harden, and ultimately result in less blood flow to crucial tissues like those of the heart. Plenty of substantiation links the relationship of LDL cholesterol in this condition and effective management requires its reduction through life style modification, complimentary methods, or medication.
Plaque Formation and LDL-Cholesterol
Complicated models abound but the basic view is that an overabundance of LDL cholesterol binds to and gathers between the lining epithelium of arteries. This LDL is collected further by local eating machines of the immune system called macrophages. LDL cholesterol is prone to becoming oxidized, especially when eaten by macrophages attempting to digest it with an enzyme called myeloperoxidase. These macrophages (often called foam cells) have a special LDL-receptor that allows them to continually eat cholesterol. This allows them to eat it until they die, leaving large pools which then attack the surrounding tissues of the artery wall. This damage occurs through the oxidative breakdown of the adjacent cell membranes and triggers further inflammatory reactions involving more macrophages.
Additional Resources
Linda T. Welson, Triglycerides And Cholesterol Research, 1st ed. (Nova Biomedical Books, 2006).
Otvos JD Cromwell WC and Cromwell WC, Otvos JD, “Low-density lipoprotein particle number and risk for cardiovascular disease,” Curr Atheroscler Rep 6, no. 5 (2004): 381–7, doi:10.1007/s11883-004-0050-5.
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