Document Detail

LXR is crucial in lipid metabolism.
MedLine Citation:
PMID:  15913974     Owner:  NLM     Status:  MEDLINE    
Liver X receptors (LXRalpha and LXRbeta) are members of the nuclear receptor superfamily and are activated by oxysterols and intermediates in the cholesterol synthetic pathway. The pivotal role of LXRs in the metabolic conversion of cholesterol to bile acids is well established. Analysis of gene expression in LXRalpha and LXRbeta deficient mice have confirmed that LXR regulates a number of target genes involved in both cholesterol and fatty acid metabolism in liver, macrophages and intestine. The observation that LXRalpha is responsive to fatty acids and is expressed in metabolic tissues suggests that it also plays a general role in lipid metabolism. Adipose tissue is the main storage site for fat in the body and plays a crucial role in overall lipid handling. Both LXRalpha and LXRbeta are expressed and activated by endogenous and synthetic ligands, which lead to lipid accumulation into adipocytes. This indicates an important regulatory role of LXR in several metabolic signaling pathways in the adipose tissue, such as glucose uptake and de novo fatty acid synthesis. Here, we review recent studies that provide new insights into the mechanisms by which LXRs act to influence fatty acid synthesis in liver and adipose tissue.
Stine Marie Ulven; Knut Tomas Dalen; Jan-Ake Gustafsson; Hilde Irene Nebb
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Prostaglandins, leukotrienes, and essential fatty acids     Volume:  73     ISSN:  0952-3278     ISO Abbreviation:  Prostaglandins Leukot. Essent. Fatty Acids     Publication Date:  2005 Jul 
Date Detail:
Created Date:  2005-06-20     Completed Date:  2005-10-20     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8802730     Medline TA:  Prostaglandins Leukot Essent Fatty Acids     Country:  Scotland    
Other Details:
Languages:  eng     Pagination:  59-63     Citation Subset:  IM    
Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, P.O. Box 1046 Blindern, N-0316 Oslo, Norway.
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MeSH Terms
Adipose Tissue / metabolism*
Cholesterol / metabolism
DNA-Binding Proteins / genetics,  metabolism*
Fatty Acids / metabolism
Lipid Metabolism*
Liver / metabolism*
Orphan Nuclear Receptors
Receptors, Cytoplasmic and Nuclear / genetics,  metabolism*
Reg. No./Substance:
0/DNA-Binding Proteins; 0/Fatty Acids; 0/Orphan Nuclear Receptors; 0/Receptors, Cytoplasmic and Nuclear; 0/liver X receptor; 57-88-5/Cholesterol

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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