Linked Life Data

12177004

Source:http://linkedlifedata.com/resource/pubmed/id/12177004

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pubmed-article:12177004pubmed:abstractTextLiver X receptors (LXR) belong to the nuclear receptor superfamily that can regulate important lipid metabolic pathways. The plasma phospholipid transfer protein (PLTP) is known to mediate transfer of phospholipids from triglyceride-rich lipoproteins to high density lipoprotein (HDL) and plays a critical role in HDL metabolism. We report here that a specific LXR agonist, T0901317, elevated HDL cholesterol and phospholipid in C57/BL6 mice and generated enlarged HDL particles that were enriched in cholesterol, ApoAI, ApoE, and phospholipid. The appearance of these HDL particles upon oral dosing of T0901317 in C57/BL6 mice was closely correlated with the increased plasma PLTP activity and liver PLTP mRNA levels. Nuclear run-on assay indicated that the effect of LXR agonist on PLTP expression was at the transcriptional level. In mouse peritoneal macrophage cells, PLTP expression was also up-regulated by the LXR/RXR (retinoid X receptor) heterodimer. However, cholesterol efflux in mouse peritoneal macrophage cells from PLTP-deficient mice (PLTP0) was not significantly different from wild type animals. Although in PLTP-deficient mice, the induction of HDL cholesterol as well as HDL particle size increase persisted, the extent of the induction was greatly attenuated. We conclude that PLTP is a direct target gene of LXRs in vivo and plays an important role in LXR agonist-mediated HDL cholesterol and size increase in mice.lld:pubmed
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pubmed-article:12177004pubmed:articleTitlePhospholipid transfer protein is regulated by liver X receptors in vivo.lld:pubmed
pubmed-article:12177004pubmed:affiliationLilly Research Laboratories, Eli Lilly & Company, Indianapolis, Indiana 46285, USA.lld:pubmed
pubmed-article:12177004pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12177004pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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