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A more recent version of this article appeared on December 1, 2004

Papers In Press, published online ahead of print September 1, 2004
J. Lipid Res., doi:10.1194/jlr.M400208-JLR200
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Submitted on June 2, 2004
Revised on August 5, 2004
Accepted on August 18, 2004

Dietary stanol esters decrease plasma cholesterol independently of changes in gene expression of intestinal ABC sterol transporters and Niemann-Pick C1 Like 1 protein in hamster

F. Jeffrey Field, Ella Born, and Satya N. Mathur

Internal Medicine, University of Iowa, Iowa City, IA 52242

Corresponding Author: f-jeffrey-field{at}uiowa.edu

Possible mechanisms for the cholesterol lowering effects of plant stanol esters were addressed by feeding hamsters diets containing stanol esters, cholesterol, or cholestyramine/lovastatin. ABCA1, ABCG1, ABCG5, ABCG8, and NPC1L1 mRNA levels were then estimated in duodenum, jejunum, and ileum. Plasma cholesterol was decreased by 36 and 94% in animals fed stanol esters and cholestyramine/lovastatin, respectively. Cholesterol feeding increased plasma cholesterol 2.5-fold. Plasma plant sterols were unchanged by stanol ester feeding but became undetectable by feeding cholestyramine/lovastatin. Cholesterol and stanols accumulated in enterocytes of animals fed cholesterol and stanol esters, respectively. ABCG5 and ABCG8 mRNA levels were decreased by stanol esters and cholestyramine/lovastatin. Cholesterol feeding markedly increased ABCA1 and ABCG1 expression while modestly increasing ABCG5/ABCG8. NPC1L1 mRNA was not significantly altered by any of the diets. ABCG1, ABCG5, ABCG8, and NPC1L1 mRNA was highest in cells of the upper villus, whereas ABCA1 mRNA was highest in cells of the lower villus. The results suggest that cholesterol lowering of stanol esters is unrelated to changes in mRNA levels of intestinal ABC sterol transporters or NPC1L1. Cholesterol flux regulates ABC expression but not NPC1L1. Different localization of ABCA1 suggests a different function for this protein than ABCG1, ABCG5, ABCG8, and NPC1L1.


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