Journal of Lipid Research, Vol 24, 1291-1303, Copyright © 1983 by Lipid Research, Inc.
Overproduction of a kinetic subclass of VLDL-apoB, and direct catabolism of VLDL-apoB in human endogenous hypertriglyceridemia: an analytical model solution of tracer data
RP Eaton, RC Allen and DS Schade
To investigate the participation of the major apoprotein involved in
triglyceride transport in the pathogenesis of endogenous
hypertriglyceridemia, five kinetic studies of apoprotein B were conducted
in volunteer normolipidemic subjects and six studies in four patients with
endogenous hypertriglyceridemia. The transport of apoprotein B within four
kinetic subclasses of very low density lipoprotein (VLDL), intermediate
density lipoprotein (IDL), and low density lipoprotein (LDL) was studied by
injection of [75Se]selenomethionine. A 24-fold increase in the entry of
newly synthesized apoprotein B at the initial kinetic subclass of the four-
compartment VLDL delipidation sequence characterized the
hypertriglyceridemic studies relative to normal subjects. Moreover,
approximately 75 mg/kg per day of VLDL-B turnover reflected direct
catabolism independent of conversion to IDL and/or to LDL, in contrast to
the 8 mg/kg per day observed in controls. IDL-B was derived from VLDL-B in
both normal and hypertriglyceridemic subjects, and was responsible for
greater than 70% of all LDL-B synthesis. LDL-B pool size and turnover were
indistinguishable in hypertriglyceridemic subjects from that observed in
normal subjects. These studies suggest that two kinetic phenomena may
characterize the pathophysiology of endogenous hypertriglyceridemia: a)
over-production of apoB within a kinetic subclass of VLDL and b)
preferential catabolism of hypertriglyceridemic VLDL without prior
conversion to IDL/LDL.
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