98 Introduction to Human Nutrition
lipolyzed by a rate-limiting lipase known as lipopro-
tein lipase (LPL). LPL is tethered to the endothelial
lining of blood vessels in peripheral tissues, most
notably muscle and adipose tissue, by proteoglycan
fi bers, and as such is known as an endothelial lipase.
Several molecules of LPL can interact and lipolyze the
TAG from a single chylomicron particle to generate a
chylomicron remnant which is removed by specifi c cell
membrane receptors in the liver. The situation is com-
plicated by the fact that TAG-rich lipoproteins from
the liver, known as very low-density lipoprotein
(VLDL), also contribute to this postprandial lipemia
to variable extents in health and disease states. These
VLDLs containing endogenously produced TAG are
similar in lipid composition to chylomicrons but con-
siderably smaller (Table 6.4). While chylomicrons
carry up to 80% of measurable plasma TAG during the
postprandial period, VLDL particles can carry up to
80% of the measurable protein (mainly as apo-B), and
signifi cantly outnumber chylomicrons at all times.
VLDL-TAG are also metabolized by LPL, which creates
competition for the clearance of endogenously and
exogenously derived TAG carried by VLDLs and chy-
lomicrons respectively.
Postprandial lipemia: relevance to
atherosclerosis
It was suggested by Zilversmit in 1979 that atheroscle-
rosis was a postprandial phenomenon. This concept
was based on the fi nding that patients either with or at
high risk of developing coronary heart disease (CHD)
showed an impaired capacity to remove TAG-rich
lipoproteins from the circulation after a meal. This
resulted in enhanced postprandial lipemia, which also
became known as the TAG intolerance hypothesis. At
about the same time, evidence emerged that TAG-rich
lipoproteins, and especially remnants of chylomi-
crons, were directly atherogenic, meaning that they
can damage the endothelial lining of arteries and
promote the deposition of cholesterol in coronary
arteries. For this reason, there is considerable research
interest in the metabolic determinants of postprandial
lipemia. This includes the mechanisms that underlie
the production and removal of TAG-rich lipoproteins,
not only in the intestine but also in the liver, since the
production and removal of VLDL can clearly infl u-
ence postprandial events. The quality and, to a lesser
extent, quantity of dietary fat are extremely important
in this respect and have a major role to play in modu-
lating lipid-mediated atherosclerosis.6.5 Circulating lipids: lipoprotein
structures and metabolismCirculating blood lipids are insoluble in water and
must be solubilized for transportation in the extracel-
lular fl uid by combining with bipolar molecules with
charged and uncharged regions (apoproteins and
phospholipids). This property, known as amphipath-
icity, enables these molecules to associate with aqueous
(hydrophilic) and nonaqueous (hydrophobic) envi-
ronments and thus renders them perfect for
enveloping insoluble lipids, chiefl y TAG and CE, in
macromolecular lipid–protein complexes called lipo-
proteins. It is worth remembering that, in the absence
of lipoproteins, TAG would exist in aqueous blood as
immiscible oil droplets, while free fatty acids liberated
from TAG and phospholipids in the absence of the
blood protein albumin would act as detergents and
dissolve cell membranes.Table 6.4 Plasma lipoproteins: classes, composition, and distribution
Chylomicrons VLDLs LDLs HDLsMass (10^6 Da) 0.4–3.0 10–100 2–3.5 0.2–0.3
Density (g/ml) >0.95 <1.006 1.02–1.063 1.063–1.210
Particle diameter (nm) > 90 30–90 22–28 5–12
Apoproteins B-48, A-I, C-I, C-II, C-III, E B-100, E B-100 A-I, A-II
Lipids % mass (molecules/particle)
Cholesterol 8 (60 000) 22 (10 000) 48 (2000) 20 (100)
Triacylglycerols 83 (500 000) 50 (24 000) 10 (300) 8 (20)
Ratio of particles
Postabsorptive 1 40 1000 10 000
Postprandial 1 25 250 250 000
VLDL, very low-density lipoprotein; LDL, low-density lipoprotein; HDL, high-density lipoprotein.