Abstract
Activity of the enzyme acyl-CoA:cholesterol acyltransferase (ACAT) in isolated rate enterocytes was reduced by approx. 75% following a single oral dose of Sandoz compound 58-035 (30 mg·kg-1). Despite this, the formation of [14C]cholesteryl esters from [1-14C]oleic acid remained unaffected in ACAT-inhibited cell preparations. The increase in serum cholesterol concentrations observed after overnight cholesterol/cholic acid ( 1% 05%) feeding to rats was abolished by pre-treatment with Sandoz compound 58-035 (30 mg·kg-1). These results can be reconciled with a previously proposed model for the transmembrane movement of cholesterol which implicates ACAT-independent esterification and hydrolysis as a transport mechanism for the movement of cholesterol across the enterocyte apical membrane.
Original language | English |
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Pages (from-to) | 213-216 |
Number of pages | 4 |
Journal | Biochimica et Biophysica Acta (BBA)/Lipids and Lipid Metabolism |
Volume | 1003 |
Issue number | 2 |
DOIs | |
Publication status | Published - 8 Jun 1989 |
Keywords
- (Rat)
- Absorption
- ACAT
- Cholesterol
- Cholesteryl ester
ASJC Scopus subject areas
- Biophysics
- Biochemistry
- Endocrinology