Tv. Fungwe et al., FATTY-ACIDS MODULATE LECITHIN-CHOLESTEROL ACYLTRANSFERASE SECRETION INDEPENDENTLY OF EFFECTS ON TRIGLYCERIDE SECRETION IN PRIMARY RAT HEPATOCYTES, The Journal of nutrition, 128(8), 1998, pp. 1270-1275
The regulation of plasma lecithin:cholesterol acyltransferase (LCAT) e
xpression is not well understood. Although oleic acid increases both t
he secretion of triglycerides and LCAT by primary rat hepatocytes, the
effect of other fatty acids (FA) on LCAT secretion is not known. This
study was designed to examine the effect of FA on the hepatic secreti
on of LCAT, triglyceride and apolipoprotein A-1 (apoA-1), Primary rat
hepatocytes were incubated with serum-free medium, supplemented with i
ndividual FA (0-1 mmol/L) for 22-24 h, Preliminary studies indicated a
linear secretion of LCAT up to 24 h in both control and FA-treated ce
lls. When hepatocytes were incubated with 1 mmol/L FA, the LCAT secret
ion increased 50-100% (P < 0.01) in the presence of the 18-carbon FA (
stearic, oleic, elaidic and linoleic acids), whereas the presence of b
utyric, lauric and palmitic acids had no significant effect. LCAT secr
etion decreased (P < 0.01) in the presence of docosahexaenoic acid (DH
A). All FA (except DHA) significantly enhanced triglyceride secretion;
however, only the 18 carbon FA significantly stimulated the synthesis
and secretion of apoA-1 and secretion of LCAT, The secretion of LCAT
correlated with apoA-1 secretion (r = 0.88, P = 0.004) but not with tr
iglyceride secretion (r = 0.55, P = 0.12). Treatment with oleic acid r
esulted in a 1.5-fold increase in hepatocyte LCAT mRNA accumulation, w
hereas butyrate and palmitate had no effect. These data indicate that
FA that promote the apparent synthesis and secretion of apoA-1 also st
imulate the secretion of LCAT in vitro, suggesting a coordinate regula
tory mechanism for apoA-1 and LCAT expression.