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Modification of dietary fatty acid composition results in
changes in plasma cholesterol levels in man. We examined the effect of
in vitro fatty acid supplementation on low density lipoprotein
(LDL) receptor activity in cultured cells and questioned whether
changes were related to fatty acid-induced alterations in
acyl-CoA:cholesterol acyltransferase (ACAT) activity. Preincubation of
cultured cells ( i.e. human skin fibroblasts, J774 macrophages,
and HepG2 cells) with oleic acid (oleic acid:bovine serum albumin molar
ratio 2:1) at 37 °C for longer than 2 h resulted in a 1.2- to
1.5-fold increase in LDL cell binding at 4 °C and LDL cell
degradation at 37 °C. Scatchard analysis showed that oleic acid
increased LDL receptor number but not LDL affinity
( K
Volume 270,
Number 17,
Issue of April 28, pp. 10008-10016, 1995
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
). Fatty acid supplementation of J774
macrophages increased both LDL receptor activity and cholesteryl ester
accumulation. The ACAT inhibitor, 58-035, eliminated both effects, and
increased ACAT activity preceded stimulation of LDL receptor activity
by 1-2 h. Supplementation of macrophages with triolein emulsion
particles also increased LDL cell binding and degradation, and addition
of cholesterol to the emulsions abolished this effect. Among fatty
acids tested, oleate (18:1), arachidonate (20:4), and eicosapentanoate
(20:5) demonstrated the greatest effects. We hypothesize that certain
fatty acids delivered to cells either in free form, or as triglyceride,
first increase cellular ACAT activity, which then causes a decrease in
an intracellular free cholesterol pool, signaling a need for increased
LDL receptor activity. This mechanism may play a role in the effect of
certain dietary fatty acids on LDL metabolism in vivo.
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