bbons 1990;268- 1-13 Spring 1992 ; 267 14839-45 Tiwari S, Siddiqi SA. 2012 May;32(5):1079-86]. The needed VLDL TGs are obtained by the liver either from de novo synthesized fatty acids (FA), a sterol family member derived via the MVA pathway [REF Cornforth 2002 24], extracted from the circulation as nonesterified FAs, or recycled from lipoprotein remnants cleared by hepatic receptors [REF Gibbons 2003 25]. Since hepatic VLDL metabolism is dependent on the availability of TG’s, the de novo synthesized APOB100 undergo degradation when they are not lipidated [REF]. Once the VLDL particles enter the circulation, an interaction with LPL in the endothelial cells reduces the TG content similar to CM degradation. The remaining VLDL remnant is deprived from TGs, intermediate-density lipoproteins (IDL), and is either removed from the circulation through hepatic clearance via the LDLr or converted by LPL and hepatic lipase (HL) into low-density lipoproteins (LDL). The LDL particle maintains the APOB100 molecule and is subjected to LDLr mediated internalization and degradation of the particle.

Subsequently, LDL derived FC is either reused for endogenous lipoprotein metabolism or excreted via the bile.

3.3.3 HDL

HDL biogenesis is a complex interaction of membrane bound and circulating plasma proteins and can be diverted into five major processes [REF Zannis 2004]. (1) Production and secretion of APOA1 by either the liver of intestine [REF Zannis 1985]. Whereas intestinal APOA1 enters the circulation via CM’s and is rapidly transferred towards HDL during hydrolysis [REF]. Hepatic derived APOA1 is the origin of nascent pre-β HDL particles Consequently targeted APOA deficiency in mice result in 83% lowering of the HDL fraction and subsequent phenotypes [REF reviewed by Hoekstra and van Eck 26] (2) Via an ABCA1 dependant pathway, hepatic APOA1 incorporates cellular phospholipids leading to the formation of lipid poor pre-βHD