A. Nagayoshi et al., ROLE OF ACYL-COENZYME-A CHOLESTEROL ACYLTRANSFERASE IN INTRAHEPATIC PROCESSING OF APO-B-LIPOPROTEIN IN SUNCUS, Journal of Biochemistry, 118(2), 1995, pp. 259-264
We have previously shown that fatty liver was easily induced in suncus
by starvation and that the plasma level of apolipoprotein B (apoB) wa
s very low, We also previously reported that a defect in the assemblin
g process of apo B-containing lipoprotein (very low density lipoprotei
n, VLDL) may be one of the reasons for the low level of plasma apo B a
nd for induction of fatty liver by starvation in suncus, We also found
that hepatic acyl coenzyme A cholesterol acyltransferase (ACAT) activ
ity is very low in the animals, resulting in decreased cholesteryl est
er contents in the liver, A deficiency of cholesteryl ester in suncus
liver may be one of the reasons for the defect in the assembling proce
ss of VLDL, In this study, we investigated the effect of cholesterol-f
eeding, which induces an increase in triglyceride and cholesteryl este
r of the liver as a consequence of the induction of both intestinal an
d hepatic ACAT activities, on the secretion of VLDL, Although the basa
l ACAT activity of intestinal mucosa was high, cholesterol-feeding did
not induce either an increase in plasma lipid or an increase in intes
tinal ACAT activities in suncus, The hepatic secretion rate of VLDL wa
s estimated by treatment with Triton WR1339, which is well known to in
hibit the catabolism of VLDL, Cholesterol-feeding caused a slight incr
ease in hepatic triglyceride and cholesteryl ester but no increase eit
her in the secretion rate of VLDL or in hepatic ACAT activity, This ev
idence suggests that either the secretion rate of VLDL is not dependen
t on absolute hepatic contents of cholesteryl ester, or it is dependen
t on the level of cholesteryl ester which is produced by hepatic ACAT.