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. 2023 Jun 26;44(39):4186–4195. doi: 10.1093/eurheartj/ehad337

Figure 4.

Figure 4

Impact of variation in genes influencing lipolysis and those influencing lipoprotein receptors on TRL/remnant and LDL metabolism. In this schematic, the putative differential effects of variants of reduced functionality are depicted in boxes. Triglyceride-rich lipoproteins remnants are defined as lipoprotein particles that have undergone partial lipolysis.2,21,22 SNPs in genes that cause a reduction in the efficiency of lipolysis (‘cluster 2’ SNPs) potentially increase the rate of TRL/remnant particle formation but have smaller effects on LDL. Since TRL/remnants contain apoB, there is a modest increment in plasma total apoB levels. Metabolic studies have established that VLDL- and chylomicron-remnants are cleared from the circulation by the LDL receptor and possibly other receptors binding to apoB on the particle surface and facilitating endocytosis and degradation.2,21 Cluster 1 SNPs which reduce the activity of the LDL receptor or alter the ligand, apoB, affect remnant clearance and cause increases in the concentration of both TRL/remnant and LDL particles with a consequent substantial rise in plasma apoB.