The lipoprotein shell contain a mono layer of phospholipids (PL), amphipathic molecules, FC and apolipoproteins [REF], enfolding the hydrophobic content of CE and triglycerides (TG) [REF]. Five lipoprotein classes are distinguished based on their buoyant density: Chylomicrons (CM), very low-density lipoprotein (VLDL), intermediate low-density lipoprotein (IDL), low-density lipoprotein (LDL) and high-density lipoprotein (HDL). The difference in lipid composition of the five lipoprotein classes is depicted in TABLE 1.

Chylomicrons are essential in the transport of exogenous cholesterol from the intestines towards the liver. Within the ER of enterocytes nascent chylomicron particles are formed as a result of lipidation of one APOB48 molecule with cellular CE, TG and phospholipids, alongside apolipoproteins [TABLE 1]. The major apolipoproteins classes are de novo synthesized by intestine and liver [REF] and located in the membrane of lipoproteins. The amphipathic apolipoproteins serve in the membrane as enzymatic cofactors and receptor ligands, regulating lipoprotein metabolism [REF 18]. The function and presence of apolipoproteins differ per lipoprotein class.

Once the chylomicrons enter the circulation via the lymphatic system, circulating APOC’s are acquired. APOC’s in the membrane of CM’s serve as a substrate for lipoprotein lipase (LPL) that is present on the endothelial cells of adipose tissue and skeletal muscle and hydrolyse the TG content for energy storage [REF goldberg 1996 19]. Upon hydrolysis, superfluous membrane phospholipids are transferred by the phospholipid transfer protein (PLTP) towards HDL. PLTP, a plasma glycoprotein and a family member of the lipopolysaccharide (LPS)-binding proteins [REF XC Jiang 1999 20], is involved in the metabolism of both the APOB lipoproteins as well as HDL. Deficiency in PLTP expression results in a marked decrease in plasma levels of