Figure 1. Dietary cholesterol is absorped in the intestine and packaged into large triglyceride (TG)-rich chylomicrons. These apolipoprotein (apo) B48-containing particles are released into the circulation in a wave following a fatty meal, and there are hydrolysed by the action of lipoprotein lipase (LpL). This enzyme, present in skeletal muscle and adipose tissue, converts lipoprotein triglyceride to fatty acids (FA). It is activated by apoCII on the surface of the particles and inhibited by apoCIII. ‘Remnants’ from LpL action are removed rapidly by the liver and the cholesterol is deposited in the organ ready for use in cellular processes or lipoprotein assembly. Synthesis from acetate is the other main source of body cholesterol. In the fasting state, very low-density lipoprotein (VLDL) particles that contain apoB100 and triglyceride are released from the liver. These are converted to low-density lipoprotein (LDL) by the action of LpL. LDL is then taken up in a regulated manner by receptors (R). When cells have sufficient cholesterol, the LDL receptor is downregulated and LDL accumulates in the bloodstream. It is eventually removed by scavenger receptors (S-R) on macrophages. In the artery wall this can lead to tissue cholesterol accumulation and atherosclerosis. Reverse cholesterol transport begins with the presentation of cholesterol at the cell surface and its transfer to apoAI (the major high-density lipoprotein (HDL) protein) by the adenosine triphosphate (ATP) binding cassette protein A1 (ABC-A1). Once esterified in HDL, the cholesterol is either transported directly to the liver or exchanged via the action of cholesteryl ester transfer protein (CETP) into VLDL and LDL.