Demonstrates stereospecific modulation of ACAT activity and cholesteryl ester synthesis by novel ketosterols in Hep G2 cells, suggesting distinct regulatory mechanisms.
Novel synthetic oxysterols (22S,23S)-3β-hydroxy-22,23-oxido-5α-ergost-8(14)-en-15-one ( I ) and (22R,23R)-3β-hydroxy-22,23-oxido-5α-ergost-8(14)-en-15-one ( II ) influenced biosynthesis of cholesteryl esters from [ 14 C]acetate (85% and 180% of control at 5 μM concentration) in the human hepatoma Hep G2 cell line. Ketosterol ( I ) increased the level of cholesteryl ester biosynthesis from [ 14 C]oleate in Hep G2 cells in a dose dependent manner, whereas the level of cholesteryl esters biosynthesis in the presence of ketosterol ( II ) reached the maximal value (269±20% of control) at 1 μM concentration of this compound. In a cell free system ketosterol ( I ) increased the rate of ACAT-dependent cholesterol acylation similar to 25-hydroxycholesterol, however, ketosterol ( II )), efficiently stimulated an initial rate of ACAT-catalyzed cholesterol esterification, followed by rapid inactivation of this enzyme.
No takes yet. Share an insight, caveat, or question.
Mehtiev et al. (2008) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: