ROLE OF ACYL-COENZYME-A CHOLESTEROL ACYLTRANSFERASE IN INTRAHEPATIC PROCESSING OF APO-B-LIPOPROTEIN IN SUNCUS

Citation
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
Citations number
38
Categorie Soggetti
Biology
Journal title
ISSN journal
0021924X
Volume
118
Issue
2
Year of publication
1995
Pages
259 - 264
Database
ISI
SICI code
0021-924X(1995)118:2<259:ROACAI>2.0.ZU;2-J
Abstract
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.