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Papers In Press, published online ahead of print March 1, 2004
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Internal Medicine, University of Iowa, Iowa City, Iowa 52242
Corresponding Author: f-jeffrey-field{at}uiowa.edu
To examine whether intestinal ABCA1 was responsible for the differences observed between cholesterol and ß-sitosterol absorption, ABCA1-facilitated ß-sitosterol efflux was investigated in CaCo-2 cells following LXR/RXR activation. Both the LXR agonist T0901317 and the natural RXR/LXR agonists, 22-hydroxycholesterol and 9-cis retinoic acid, enhanced the basolateral efflux of ß-sitosterol without altering apical efflux. LXR-mediated enhanced ß-sitosterol efflux occurred between 6 and 12 hr after activation suggesting that transcription, protein synthesis, and trafficking was likely necessary prior to facilitating efflux. The transcription inhibitor, actinomycin D, prevented the increase in ß-sitosterol efflux by T0901317. Glybenclamide, an inhibitor of ABCA1 activity, and arachidonic acid, a fatty acid that interferes with LXR activation, also prevented ß-sitosterol efflux in response to LXR ligand activation. Influx of ß-sitosterol mass did not alter the basolateral or apical efflux of the plant sterol nor did it alter ABCA1, ABCG1, ABCG5, ABCG8 gene expression or ABCA1 mass. Similar to results observed with intestinal ABCA1-facilitated cholesterol efflux, LXR/RXR ligand activation enhances the basolateral efflux of ß-sitosterol without affecting apical efflux. The results suggest that ABCA1 does not differentiate between cholesterol and ß-sitosterol and thus, is not responsible for the selectivity of sterol absorption by the intestine. ABCA1, however, may play a role in ß-sitosterol absorption.
Revised on January 31, 2004
Accepted on February 20, 2004
LXR/RXR ligand activation enhances the basolateral efflux of
-sitosterol in CaCo-2 cells
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