which are end-products of the intravascular
metabolism of VLDLs. The LDLs, which are
rich in cholesterol esters and phospho-
lipids, are taken up by receptors in the
skeleton, intestine, liver, adrenals and
corpus luteum (Fig. 5.2).
The HDLs are synthesized and
secreted by the liver and small intestine as
small discoidal particles consisting of a
phospholipid bilayer containing only apo-A
and free cholesterol (Fielding and Fielding,
1995). The particles become spherical as
cholesterol esters are formed via the
lecithin–cholesterol acyltransferase (LCAT)
reaction (Fig. 5.2). This enzyme, synthe-
sized in liver and secreted into plasma,
binds to the discoidal HDLs and catalyses
the transfer of a fatty acid (usually linoleic
acid) from the sn-2 position of lecithin
(phosphatidylcholine) to free cholesterol,
forming cholesterol esters and lysolecithin.
The non-polar cholesterol esters move into
the interior of the particle, causing it to
become spherical and to enlarge as more
cholesterol ester is formed. Lysolecithin is
transferred to albumin in plasma. The
HDLs acquire excess surface components
(phospholipids, apo-C, apo-E) from VLDLsLipid Metabolism 103Fig. 5.2.Schematic diagram of lipoprotein metabolism in farm animals. Chylomicrons or very low-density
lipoproteins (VLDLs) secreted from the intestine or liver acquire apoprotein CII (apo-CII) from newly secreted
(nascent) high-density lipoproteins (HDLs). Triacylglycerols in chylomicrons or VLDLs are hydrolysed by
lipoprotein lipase (LPL) in peripheral tissues, which is activated by apo-CII and allows fatty acid uptake by
tissues. The remaining particles (remnants or intermediate-density lipoproteins, IDLs) are cleared by the liver
or undergo further triacylglycerol hydrolysis to produce low-density lipoproteins (LDLs). Excess surface com-
ponents (phospholipids, PLs; apoproteins C and A; free cholesterol, chol) are transferred to HDLs. LDLs are
degraded in the liver or after receptor-mediated uptake in peripheral tissues. HDLs take up excess cholesterol
(chol) from peripheral tissues and convert it to cholesterol esters by the action of lecithin cholesterol acyl-
transferase (LCAT); lysolecithin is released into plasma, and cholesterol esters enter the core of HDLs. HDLs
can deliver cholesterol to tissues or return it to the liver for conversion to bile salts. In some species,
cholesterol esters may be transferred from HDLs to LDLs by cholesterol ester transfer protein.