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Papers In Press, published online ahead of print February 20, 2001
Department of Internal Medicine, UT Southwestern Medical Center at Dallas, Dallas, TX 75390-8887
Corresponding Author: spady{at}utsw.swmed.edu
Cholesterol acquired by extrahepatic tissues (from de novo synthesis or lipoproteins) is returned to the liver for excretion in a process called reverse cholesterol transport (RCT). We undertook studies to determine if RCT could be enhanced by upregulating individual steps in the RCT pathway. Overexpression of 7a-hydroxylase, Scavenger receptor B1 (SR-BI), lecithin cholesterol acyltransferase (LCAT) or apo AI in the liver did not stimulate cholesterol efflux from any extrahepatic tissue. In contrast, infusion of apo AI/phospholipid complexes (rHDL) that resemble nascent HDL markedly stimulated cholesterol efflux from tissues into plasma. Cholesterol effluxed to rHDL was initially unesterified but by 24 h this cholesterol was largely esterified and had shifted to normal HDL (in mice lacking cholesteryl ester transfer protein, CETP) or to apo B containing lipoproteins (in CETP transgenic mice). Most of the cholesterol effluxed into plasma in response to rHDL came from the liver. However, an even greater proportion of effluxed cholesterol was cleared by the liver resulting in a transient increase in liver cholesterol concentrations. Fecal sterol excretion was not increased by rHDL. Thus, although rHDL stimulated cholesterol efflux from most tissues and increased net cholesterol movement from extrahepatic tissues to the liver, cholesterol flux through the entire RCT pathway was not increased.
J. Biol. Chem, 10.1074/jbc.M010230200
Submitted on November 9, 2000
Revised on February 8, 2001
Accepted on February 18, 2001
Effect of upregulating individual steps in the reverse cholesterol transport pathway on reverse cholesterol transport in normolipidemic mice
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