Diagnosis and Assessment of Disease Figure 6. LDL Particle Composition
Factors Affecting Lipoprotein Core Lipid Composition (Figs 4 and 5)
ÎTG-rich lipoproteins, using cholesteryl ester transfer protein (CETP), exchange TG for CE molecules leading to TG-rich and CE-poor LDL and HDL, and TG-poor and CE-rich VLDLs.
ÎThis, in turn, leads to reductions in LDL-C and HDL-C and elevations in VLDL-C and non-HDL-C.
ÎThe TG-rich and CE-poor LDL and HDL, upon exposure to hepatic lipase, lose TG and surface phospholipids and become smaller LDL and HDL particles.
• Small LDL particles have delayed clearance by LDL receptors. ▶ This increases small LDL-P and total LDL-P (and apoB). ▶ The small HDL-P are subject to catabolism and metabolism of apoA-I by the kidneys, leading to reductions in HDL-P, apoA-I, and HDL-C.
• With rare exceptions (Type I, III, V lipoprotein disorders), over 90% of apoB particles are LDL.
• Characteristically, such patients have high apoB (LDL-P and VLDL remnants) and low apoA-I (total HDL-P) (elevated apoB/apoA-I or LDL-P/HDL-P ratios).
• Until proven otherwise, assume that patients with low HDL-C have too many LDL particles (elevated apoB and LDL-P) and reduced large HDL-P.
• Increased large VLDL-P and VLDL size, increased small LDL-P, decreased LDL size, decreased HDL size and large HDL-P are lipoprotein markers of insulin resistance.
ÎHigh TG and reduced HDL-C are characteristically accompanied by elevated apoB (> 90% of these being LDL particles), elevated LDL-P, and reduced apoA-I (HDL-P).
6
