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Journal of Lipid Research, Vol 26, 852-859, Copyright © 1985 by Lipid Research, Inc.
F Berr, R Eckel and F Kern Jr
In an earlier study it was shown that retinyl palmitate appeared to be a
satisfactory label for the core of chylomicrons and their remnants. When
chylomicrons were endogenously labeled with retinyl palmitate and
pulse-injected into healthy donors, retinyl palmitate was cleared from
plasma by a first order process. Its fractional decay constant was very
similar to the fractional catabolic rate of VLDL triglycerides, a
lipoprotein lipase-dependent process, and 2-3 times slower than hepatic
chylomicron remnant uptake in experimental animals. We, therefore,
investigated whether plasma clearance of retinyl palmitate-labeled
chylomicrons is accelerated by enhanced plasma triglyceride hydrolysis
produced by heparin administration. Five healthy subjects took retinyl
palmitate by mouth and 5-6 hr later two units of plasma were obtained by
plasma-pheresis. After storage for 42 hr, the units were pooled and
separated into two equal volumes. The first half was injected into the
donor and plasma retinyl palmitate and chylomicron triglyceride were
measured for 3.5 hr (control study). Heparin was then given intravenously
as a bolus followed by an infusion for 7 hr. A second retinyl palmitate
clearance (postheparin study) was performed during the heparin infusion.
Plasma lipolytic activity and retinyl palmitate and chylomicron
triglyceride concentrations were measured serially. Total plasma lipolytic
activity and hepatic triglyceride lipase activity were increased
approximately 500-fold during postheparin studies, enhancing triglyceride
decay 2.5- to 3-fold. Retinyl palmitate plasma decay, however, was
unaffected. Retinyl palmitate plasma decay was a biexponential
concentration-dependent function in eighty of ten pre- and postheparin
studies with the first, rapid exponential accounting for 90 +/- 4% of total
plasma retinyl palmitate decay.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Plasma decay of chylomicron remnants is not affected by heparin- stimulated plasma lipolytic activity in normal fasting man
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