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Journal of Lipid Research, Vol 36, 158-171, Copyright © 1995 by Lipid Research, Inc.
A Gaw, CJ Packard, GM Lindsay, BA Griffin, MJ Caslake, AR Lorimer and J Shepherd
An analysis of apolipoprotein (apo) B turnovers conducted in subjects with
moderate hypercholesterolemia was performed to discover relationships that
may exist between apoB kinetic parameters and plasma lipid and lipoprotein
levels. A group of 21 subjects with plasma cholesterol in the range 250-300
mg/dl and triglyceride < 265 mg/dl were injected with tracers of
131I-labeled very low density lipoprotein 1 (VLDL1, Sf 60-400) and
125I-labeled VLDL2 (Sf 20-60) prepared by cumulative flotation
ultracentrifugation. The metabolism of apoB in these fractions was followed
through intermediate density (IDL, Sf 12- 20) to low density (LDL, Sf 0-12)
lipoprotein. The most consistent feature giving rise to the higher apoB
levels that occurred in VLDL2, IDL, and LDL in the hypercholesterolemic
group was increased input of VLDL2 (787 +/- 607 (SD) mg/day vs. 349 +/- 213
in normals, P < 0.01). VLDL1 apoB input was variably affected and not
significantly different from normal. However, the plasma residence time of
this subfraction was increased (0.15 +/- 0.07 days vs. 0.08 +/- 0.03 days
in normals, (P < 0.001) due to a decreased fractional rate of direct
catabolism. Fractional transfer rates (FTR) down the delipidation cascade
and other fractional rates of direct catabolism were, overall, not
significantly different from normal. The plasma residence time of VLDL2
apoB and LDL apoB was similar in hypercholesterolemic and normal subjects,
while that of IDL apoB was slightly increased. Variation in LDL apoB mass
within the hypercholesterolemic group correlated with VLDL1 apoB input (r =
0.58, P = 0.006), the fractional rate of transfer from IDL to LDL (r =
0.61, P = 0.003), and direct LDL input (r = 0.64, P = 0.002). The
proportion of LDL apoB mass derived by direct, i.e., VLDL-independent
input, varied from 5 to 50% and was inversely correlated with plasma
triglyceride (r = -0.53, P = 0.014) and positively with HDL2 (r = 0.66, P =
0.002). In addition, the amount of direct LDL input was related to the
amount of VLDL1 removed by direct catabolism (r = 0.53, P = 0.013). The
analysis indicated that moderate hypercholesterolemia arose principally
from overproduction of small VLDL, while variation in VLDL1 input and the
IDL to LDL conversion rate (presumably hepatic lipase- mediated) modulated
the extent of the elevation in LDL apoB.
ARTICLES
Overproduction of small very low density lipoproteins (Sf 20-60) in moderate hypercholesterolemia: relationships between apolipoprotein B kinetics and plasma lipoproteins
Institute of Biochemistry, Glasgow Royal Infirmary, UK.
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