Abstract
Plant stanols and sterols of the 4-desmethyl family (e.g., sitostanol and sitosterol) effectively decrease LDL cholesterol concentrations, whereas 4,4-dimethylsterols (alpha-amyrin and lupeol) do not. Serum carotenoid concentrations, however, are decreased by both plant sterol families. The exact mechanisms underlying these effects are not known, although effects on micellar composition have been suggested. With a liver X receptor (LXR) coactivator peptide recruitment assay, we showed that plant sterols and stanols from the 4-desmethylsterol family activated both LXRalpha and LXRbeta, whereas 4,4-dimethyl plant sterols did not. In fully differentiated Caco-2 cells, the functionality of this effect was shown by the increased expression of ABCA1, one of the known LXR target genes expressed by Caco-2 cells in measurable amounts. The LXR-activating potential of the various plant sterols/stanols correlated positively with ABCA1 mRNA expression. Reductions in serum hydrocarbon carotenoids could be explained by the effects of the 4-desmethyl family and 4,4-dimethylsterols on micellar carotenoid incorporation. Our findings indicate that the decreased intestinal absorption of cholesterol and carotenoids by plant sterols and stanols is caused by two distinct mechanisms.
Highlights
Plant stanols and sterols of the 4-desmethyl family effectively decrease LDL cholesterol concentrations, whereas 4,4-dimethylsterols (␣-amyrin and lupeol) do not
ABCA1 is not related to intestinal cholesterol absorption, this gene was chosen because the Caco-2 cells did not express ABCG5 and ABCG8, which are involved in cholesterol absorption, at detectable levels
Foods enriched with plant stanols and sterols potently decrease serum LDL cholesterol concentrations as a result of effects in the intestinal lumen or within enterocytes
Summary
Plant stanols and sterols of the 4-desmethyl family (e.g., sitostanol and sitosterol) effectively decrease LDL cholesterol concentrations, whereas 4,4-dimethylsterols (␣-amyrin and lupeol) do not. Numerous intervention trials have demonstrated that plant stanol/sterol esters consistently and dosedependently decrease serum LDL cholesterol concentrations in various populations and patient groups [2] The mechanism underlying this hypocholesterolemic effect is a reduction in cholesterol absorption from the intestinal lumen into the circulation, as explained through a competition between plant stanols/sterols and intestinal cholesterol for incorporation into mixed micelles [3]. In contrast to the 4-desmethylsterols such as sitostanol and sitosterol, 4,4-dimethylsterols such as lupeol and ␣-amyrin (Fig. 1) decrease only serum carotenoid concentrations [14] This suggests that the mechanisms underlying the reductions in serum LDL cholesterol and carotenoid concentrations are different. That LXR activation by synthetic LXR ligands [15,16,17] increases intestinal ABCA1 as well as ABCG5 and ABCG8 expression and decreases intestinal cholesterol absorption [10, 15, 17]
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