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.
|Number of pages||4|
|Journal||Biochimica et Biophysica Acta (BBA)/Lipids and Lipid Metabolism|
|Publication status||Published - 8 Jun 1989|
- Cholesteryl ester