Fig. 2.

Role of HDL in lipoprotein metabolism. Apo A1, the main protein in HDL, is formed in the liver and the small intestine and secreted as lipid-free pre-ß-HDL. Pre-b-HDL can also come from chylomicron metabolism, or from the interconversion of HDL itself. Their interaction with ATP-binding cassette transporter A1 (ABCA1) leads to the efflux of phosphatidylcholine (PC) and free cholesterol (FC), and thus to the formation of disc-shaped HDL. Esterification of the free cholesterol by lecithin–cholesterol acyltransferase (LCAT) leads to the formation of mature spherical HDL. The lipid-rich discoidal and spherical HDL enable passive diffusion out of cells, which is facilitated by ATP-binding cassette transporter G1 (ABCG1), scavenger receptor class B type I (SR-B1) and by cholesterol esterification mediated by LCAT. Cholesteryl ester transfer protein (CETP) transfers cholesteryl esters (CE), triglycerides and phospholipids (PL) between HDL, LDL and VLDL. It thereby contributes to the formation of LDL, which is taken up through LDL receptors (LDLR) in hepatocytes. Phospholipid transfer protein (PLTP) belongs to the same protein family as CETP. Its function is to transport phospholipids between HDL and VLDL, and between various HDL. Mediated by SR-BI, HDL can deliver cholesteryl ester (and free cholesterol) to hepatocytes, steroid-producing cells and adipocytes. With permission of Springer [7]