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Papers In Press, published online ahead of print April 1, 2005
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Pathology, Wake Forest Univ. Health Sciences, Winston-Salem, NC 27157
Corresponding Author: lrudel{at}wfubmc.edu
The relative contributions of ACAT2 and LCAT to the CE content of VLDL and LDL were measured. ACAT2 deficiency led to a significant decrease in the percent CE (37.2±2.1% vs. 3.9±0.8%) in plasma VLDL, with a concomitant increase in the percent of TG (33.0±3.2% vs. 66.7±2.5%). Interestingly, the absence of ACAT2 had no apparent effect on the percentage CE in LDL, whereas LCAT deficiency significantly decreased the CE percentage (38.6±4.0% vs 54.6±1.9%) and significantly increased the percentage phospholipids (11.2±0.9% vs. 19.3±0.1%) of LDL. When both LCAT and ACAT2 were deficient, VLDL composition was similar to VLDL of the ACAT2 deficient mouse, while LDL were depleted in core lipids and enriched in surface lipids, appearing discoidal when observed by electron microscopy. We conclude that ACAT2 is important in synthesis of VLDL CE, while LCAT is important in remodeling of VLDL to LDL. Liver perfusions were performed and perfusate apoB accumulation rates in ACAT2 deficient mice were not significantly different from controls; perfusate VLDL CE decreased from 8.0 ± 0.8% in controls to 0 ± 0.7% in ACAT2 deficient mice. In conclusion, our data establish that ACAT2 provides core CE of newly secreted VLDL, while LCAT adds CE during LDL particle formation.
Revised on March 1, 2005
Accepted on March 16, 2005
ACAT2 contributes cholesteryl esters to newly secreted VLDL while LCAT adds CE to LDL in mice
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