Fig. 3.

Schematic representation of HDL functional assays in RCT pathway. Hepatocytes, enterocytes and macrophages express ATP-binding cassette (ABC) transporter A1 (ABCA1), which effluxes phospholipids and cholesterol (assay 8) and thereby lipidates apoA-I extracellularly (assays 2–3). Effluxed (FC) is modified by the HDL enzyme (LCAT) into (CE) (assays 6–7). The initially smaller HDL₃ (assays 1–2–3–4–5) particles grow in size by ongoing lipid efflux, and cholesterol esterification. The resulting HDL₂ (assays 1–2–3–4–5) particles deliver lipids to the liver, either directly via SR-BI and indirectly via CETP mediated transfer of CE to VLDL and LDL (assays 1–4–5). The RCT is finalized by the biliary excretion of cholesterol from the liver into the intestine either directly via ABCG5 and ABCG8 to bile acids via the bile salt export pump ABCB11 (assays 10–11). The actions of hepatic lipase (HL), and endothelial lipase (EL) on HDL₃, as well as of PLTP on HDL₂, liberate lipid-free apoA-I (assays 2–3). Lipid free apoA-I is either used for de novo formation of mature HDL particles or is filtrated through the renal glomerulus for tubular uptake and degradation (dotted arrows). Numbers in rectangles refer to Table 2, Table 3.