Interrelationships among serum triacylglycerols and low- and high-density lipoproteins
Lipids are constantly moving between lipoprotein particles. This movement is not totally random but influenced by the relative lipid composition of the lipoproteins and by specific lipid transfer proteins (LTPs) that act as lipid shuttles. In a normal, healthy individual, TAG-rich lipoproteins transfer TAG to LDL and HDL in equimolar exchange for CE.
This is mediated through an LTP called cholesteryl transfer protein (CETP). In this way, CEs are transferred from HDL to VLDL for passage back to the liver. Conversely, when the concentration of serum TAG and thus TAG-rich lipoproteins is increased, for example by either the overproduction of TAG in the liver or the impaired removal of TAG by LPL, the result is a net transfer of TAG into LDL and HDL. As LDL and HDL are over-loaded with TAG they become favored substrates for the action of HL and are remodeled into smaller and denser particles. While small, dense HDL is catabo-lized rapidly in the liver, lowering serum HDL and impairing reverse cholesterol transport, small, dense
LDLs are removed less effectively by LDL receptors and accumulate in serum. Small, dense LDL, by virtue of its size, has a much greater potential to infiltrate the artery wall and deposit its cholesterol. Even a moderately raised concentration of serum TAG (>1.5 mmol/l) may be inversely associated with reduced HDL cholesterol (<1 mmol/l) and a predomi-nance of small, dense LDL. This collection of findings is known as the atherogenic lipoprotein phenotype (ALP) and is a very common but modifiable source of increased CHD risk in free-living populations.
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