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Abstract
Small (Sf 20–100) very low density lipoprotein (VLDL) particles were prepared by density gradient
ultracentrifugation of plasma from normolipidemic and type IV hypertriglyceridemic
post-infarction patients and healthy controls. The small VLDL separated from the plasma
of severely hypertriglyceridemic post-infarction patients were found to contain twice
the amount of cholesteryl esters per particle, compared with small VLDL from normolipidemic
patients and healthy controls. There was a linear increase in the percentage of cholesterol
that was esterified in the small VLDL with the serum VLDL triglyceride concentration
(r = 0.66). When incubated for two hours with bovine lipoprotein lipase in excess
and bovine albumin as a free fatty acid acceptor at one and the same triglyceride
concentration in the medium, the end-product isolated by ultracentrifugation varied
as a function of the serum VLDL triglyceride level. The amount of glyceride-glycerol
recovered after two hours of incubation with lipoprotein lipase was 13.3 ± 1.3% (mean
± SEM) of the initial values and did not correlate with the VLDL triglyceride level.
With rising serum VLDL triglyceride concentration, the product isolated in the low
density lipoprotein (LDL) density region (1.006 < d < 1.063 kg/1) contained more total cholesterol and phospholipids. The linear correlation
coefficients for these relations were 0.65 and 0.58 for cholesterol and phospholipids
respectively. The ratio of total cholesterol to insoluble protein in the LDL density
range after lipolysis rose with increasing serum VLDL triglyceride level (r = 0.68). The end-product was further characterized by density gradient ultracentrifugation
of the incubate. In vitro LDL derived by lipolysis of normolipidemic small VLDL was
denser than in vitro LDL of hypertriglyceridemic small VLDL. A significant relation
was found between the percentage of cholesteryl esters of total cholesterol in the
substrate and the relative amount of total cholesterol recovered in the LDL density
fraction after lipolysis (r = 0.69). We suggest that the enrichment with cholesteryl esters of small VLDL from
type IV hypertriglyceridemic patients is caused by lipid transfer from LDL and high
density lipoprotein (HDL) and that the change in VLDL particle composition influences
the precursor-product relationship to LDL.
Keywords
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Article info
Publication history
Accepted:
February 1,
1990
Received in revised form:
January 15,
1990
Received:
July 17,
1989
Identification
Copyright
© 1990 Published by Elsevier Inc.