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Papers In Press, published online ahead of print September 8, 2005
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Pathology, Section on Comparative Medicine, Wake Forest University Health Sciences, Winston-Salem, NC 27157
Corresponding Author: rtemel{at}wfubmc.edu
The process of cholesterol absorption has yet to be completely defined at a molecular level. Due to its ability to esterify cholesterol for packaging into nascent chylomicrons, acyl-CoA:cholesterol O-acyltransferase 2 (ACAT2) plays an important role in cholesterol absorption. However, it has been found that cholesterol absorption is not completely inhibited in ACAT2 deficient mice (ACAT2 KO). Since ATP-binding cassette transporter A1 (ABCA1) mRNA expression was increased 3 fold in the small intestine of ACAT2 KO mice, we hypothesized that ABCA1-dependent cholesterol efflux sustains cholesterol absorption in the absence of ACAT2. To test this hypothesis, cholesterol absorption was measured in mice deficient in both ABCA1 and ACAT2 (DKO). Compared to wild type, ABCA1 KO, or ACAT2 KO mice, the DKO mice displayed the lowest level of cholesterol absorption. The concentrations of hepatic free and esterified cholesterol and gall bladder bile cholesterol were significantly reduced in the DKO compared to the wild type and ABCA1 KO mice although these measures of hepatic cholesterol metabolism were very similar in the DKO and ACAT2 KO mice. It was concluded that ABCA1, especially in the absence of ACAT2, can have a significant effect on cholesterol absorption although ACAT2 has a more substantial role in this process than ABCA1.
Revised on August 4, 2005
Accepted on August 17, 2005
Intestinal cholesterol absorption is substantially reduced in mice deficient in both ATP-binding cassette transporter A1 (ABCA1) and Acyl-CoA:Cholesterol O-acyltransferase 2 (ACAT2)
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