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J. Biol. Chem., Vol. 276, Issue 46, 43018-43024, November 16, 2001
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From the Department of Pharmacology and Howard Hughes Medical
Institute, University of Texas Southwestern Medical Center, Dallas,
Texas 75390-9050
Lipoprotein lipase (LPL) is a key enzyme for
lipoprotein metabolism and is responsible for hydrolysis of
triglycerides in circulating lipoproteins, releasing free fatty
acids to peripheral tissues. In liver, LPL is also believed to promote
uptake of high density lipoprotein (HDL)-cholesterol and thereby
facilitate reverse cholesterol transport. In this study we show that
the Lpl gene is a direct target of the oxysterol liver X
receptor, LXR The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) M63335 (51).
Regulation of Lipoprotein Lipase by the Oxysterol Receptors,
LXR
and LXR
*
,, and
. Mice fed diets containing high cholesterol or an
LXR-selective agonist exhibited a significant increase in LPL
expression in the liver and macrophages, but not in other tissues
(e.g. adipose and muscle). Studies in
Lxr-deficient mice confirmed that this response was dependent more on the presence of LXR than LXR
. Analysis of the
Lpl gene revealed the presence of a functional DR4 LXR
response element in the intronic region between exons 1 and 2. This
response element directly binds rexinoid receptor (RXR)/LXR
heterodimers and is sufficient for rexinoid- and LXR agonist-induced
transcription of the Lpl gene. Together, these studies
further distinguish the roles of LXR and and support a growing
body of evidence that LXRs function as key regulators of lipid
metabolism and are anti-atherogenic.
*
This work was funded by the Howard Hughes Medical Institute
(HHMI) and grants from the Robert A. Welch Foundation, the Human Frontier Science Program, and the National Institutes of Health (Specialized Programs of Research Excellence in Lung Cancer).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Research Associates of the HHMI.
§
An Investigator of the HHMI. To whom correspondence should be
addressed: HHMI, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9050. Tel.: 214-648-6349; Fax:
214-648-5419; E-mail: davo.mango@utsouthwestern.edu.
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