Journal of Lipid Research, Vol 30, 347-355, Copyright © 1989 by Lipid Research, Inc.
A novel explanation for the reduced LDL cholesterol in severe hypertriglyceridemia
A Minnich, BG Nordestgaard and DB Zilversmit
Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853.
When [3H]cholesteryl ester-labeled low density (LDL) and intermediate
density lipoproteins (IDL) from a normotriglyceridemic,
hypercholesterolemic rabbit were injected into severely
hypertriglyceridemic, hypercholesterolemic rabbits, 60% of the label
appeared in very low density lipoproteins (VLDL) at 3 hr. A similar
experiment showed that 40% of injected 131I-protein-labeled LDL appeared in
the IDL fraction at 4 hr. Taken together, these data suggest that the
exchange of LDL cholesteryl ester for VLDL triglyceride results in a
density shift of injected LDL to the IDL density range. Furthermore, the
percent of injected 131I-labeled LDL from normotriglyceridemic rabbits that
appeared in the IDL fraction increased in rabbits with increasing levels of
plasma triglyceride. This LDL density shift was reproduced in vitro by
incubating iodinated LDL from normotriglyceridemic, hypercholesterolemic
rabbits with concentrations of VLDL from hypertriglyceridemic,
hypercholesterolemic rabbits similar to those in plasma. With such a
system, it was shown that the percentage of LDL that appeared in the IDL
fraction increased with time, was enhanced fourfold by the addition of
plasma lipid transfer protein, increased with increasing molar ratio of
triglyceride to cholesteryl ester in VLDL, but apparently did not increase
with increasing VLDL particle number. These studies suggest that a
pronounced decrease in density of lipoproteins that would normally appear
in the LDL density range, resulting from loss of cholesteryl ester in
exchange for VLDL triglyceride, may explain, at least in part, the reduced
LDL levels in severe hypertriglyceridemia.
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