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11
| 3 | 2009
Klinisk Biokemi i Norden
including 33,400 individuals, and compared with
fasting levels, total cholesterol, low density lipo-
protein (LDL) cholesterol, high density lipoprotein
(HDL) cholesterol, and albumin levels were reduced
up to 3-5 hours after the last meal, triglycerides levels
were increased up to 6 hours after the last meal,
while non-HDL cholesterol, apolipoprotein A1, and
apolipoprotein B levels did not change in response to
normal food intake (8). After adjustment for albumin
levels and thus for hemodilution due to fluid intake,
total and LDL cholesterol levels no longer changed in
response to normal food intake; however, triglycer-
ides still increased modestly.
In agreement with these results, data from
26,330 women from the Women’s Health Study
found no substantial changes in the distributions
of lipids, lipoproteins, and apolipoproteins as a fun-
ction of time since the last meal, except for trigly-
cerides (7). The highest levels of triglycerides were
observed 4-5 hours postprandially, exactly as seen in
Figure 1.
Remnant lipoprotein cholesterol
and nonfasting triglycerides
Remnant lipoproteins can be defined and measured
in many sophisticated ways, all likely more precise
than the definition used in two recent papers (9,11).
However, these papers used the simplest possible
definition, one that can be used by any clinician as
long as lipid profile measurements are performed
in the nonfasting state: remnant lipoprotein choles-
terol can be calculated as nonfasting total cholesterol
minus nonfasting LDL cholesterol minus nonfasting
HDL cholesterol.
This calculation of remnant lipoprotein choleste-
rol includes remnants from chylomicrons as well as
remnants from very low density lipoprotein (VLDL).
Because degradation of triglycerides in chylomicrons
and VLDL begins immediately after these particles
are released into plasma, practically all triglyceride-
rich lipoproteins in plasma can be classified as rem-
nants, except in the rare case of familial lipoprotein
lipase deficiency with chylomicronemia seen in 1 in
a million. In other words, this definition of remnant
lipoprotein cholesterol includes cholesterol in all
triglyceride-rich lipoproteins.
The increase in nonfasting triglycerides seen after
normal food intake was mimicked by an increase in
remnant lipoprotein cholesterol (Figure 1). In accor-
Figure 2.
Levels of remnant lipoprotein cholesterol as a func-
tion of levels of nonfasting triglycerides. Values are medians
and interquartile ranges. These levels were measured in par-
ticipants from the general population, the Copenhagen City
Heart Study, who had nonfasting triglycerides and remnant
lipoprotein cholesterol measured at the 1991-1994 examina-
tion. Modified from Nordestgaard et al. JAMA 2007; 298:
299-308.
dance with this, the measured levels of nonfasting tri-
glycerides after normal food intake marked increased
levels of cholesterol in remnant lipoproteins in both
women and men (Figure 2)(9).
Nonfasting triglycerides and myocardial
infarction
In a prospective study with 26 years follow-up of
13,000 individuals from the Danish general popula-
tion, the Copenhagen City Heart Study, nonfasting
triglycerides ≥5 mmol/L predicted a 17 and 5 fold risk
of myocardial infarction inwomen andmen (Figure 3)
(9). Because most previous studies (13-15) have
focused on fasting levels of triglycerides that exclude
remnant lipoproteins, and studied mainly tertiles or
quartiles rather than very high levels of triglycerides,
the demonstrated predictive ability of nonfasting
triglycerides ≥5 mmol/L has previously gone unno-
ticed. Also, the association between stepwise increas-
es in levels of nonfasting triglycerides and stepwise
increases in risk of myocardial infarction with no
threshold effect was previously undetected.
Importantly, a simultaneously published paper
from the Women’s Health Study found that upper
versus lower tertiles or quintiles of nonfasting trig-
lycerides, but not fasting levels, associated with
(Fortsætter side 12)
<1
1-1.99 2-2.99 3-3.99 4-4.99 ≥5
