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J. Lipid Res.
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A more recent version of this article appeared on September 1, 2003

Papers In Press, published online ahead of print June 16, 2003
J. Lipid Res., doi:10.1194/jlr.M300164-JLR200
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Submitted on April 21, 2003
Revised on June 10, 2003
Accepted on June 10, 2003

Quantitation of two pathways for cholesterol excretion from the brain in normal mice and mice with neurodegeneration

Chonglun Xie, Erik G. Lund, Stephen D. Turley, David W. Russell, and John M. Dietschy

Internal Medicine, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390-8887

Corresponding Author: john.dietschy{at}utsouthwestern.edu

Although the pool of cholesterol in the adult central nervous system is large and of constant size, little is known of the process(es) involved in regulation of sterol turnover in this pool. In 7 week old mice, net excretion of cholesterol from the brain equaled 1.4 mg/d per kg body weight, and from the whole animal was 179 mg/d per kg. Deletion of cholesterol 24-hydroxylase, an enzyme highly expressed in the CNS, did not alter brain growth or myelination, but reduced sterol excretion from the CNS 64%, to 0.5 mg/d per kg. In mice with a mutation in the Niemann-Pick C gene that had ongoing neurodegeneration, sterol excretion from the CNS was increased to 2.3 mg/d per kg. Deletion of cholesterol 24-hydroxylase activity in these animals reduced net excretion only 22%, to 1.8 mg/d per kg. Thus, at least two different pathways promote net sterol excretion from the CNS. One uses cholesterol 24-hydroxylase and may reflect sterol turnover in large neurons in the brain. The other probably involves the movement of cholesterol or one of its metabolites across the blood-brain barrier and may more closely mirror sterol turnover in pools such as glial cell membranes and myelin.


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