Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Record number 360312
Title PPAR - and dyslipidemia
Author(s) Duval, C.N.C.; Müller, M.R.; Kersten, A.H.
Source Biochimica et Biophysica Acta. Molecular and Cell Biology of Lipids 1771 (2007)8. - ISSN 1388-1981 - p. 961 - 971.
Department(s) Chair Nutrition Metabolism and Genomics
Publication type Refereed Article in a scientific journal
Publication year 2007
Keyword(s) proliferator-activated-receptor - coronary-artery-disease - low-density-lipoprotein - apolipoprotein-c-iii - rev-erb-alpha - diabetes atherosclerosis intervention - reverse cholesterol transport - angiopoietin-like protein-4 - chylomicron-like emulsions - coenzyme
Abstract Dyslipidemia is defined by abnormal levels of plasma lipoproteins. Several different types of dyslipidemia can be distinguished. An important group of drugs used in the treatment of dyslipidemia are the fibrates. Fibrates serve as agonists for the peroxisome proliferator-activated receptor alpha (PPAR¿), a ligand-activated transcription factor that belongs to the superfamily of nuclear hormone receptors. By binding to response elements mostly present in the promoter of target genes, PPAR¿ governs the expression of numerous genes involved in a variety of metabolic processes. Activation of PPAR¿ results in a reduction of plasma TG levels, which is achieved by: (1) induction of genes that decrease the availability of TG for hepatic VLDL secretion, and (2) induction of genes that promote lipoprotein lipase-mediated lipolysis of TG-rich plasma lipoproteins. The stimulatory effect of PPAR¿ on plasma HDL levels in humans, which is opposite to what is observed in mice, appears to be mainly mediated via increased production of APOA1 and APOA2, the apolipoprotein constituents of HDL. Apart from its major actions outlined above, PPAR¿ modulates lipoprotein metabolism in several other ways, mostly via direct up-regulation of specific PPAR¿ target genes. By taking into account novel insights into the metabolism of plasma lipoproteins and by considering the latest information on PPAR¿-dependent gene regulation, a fresh perspective on the molecular mechanisms underlying the plasma lipoprotein modulating effect of PPAR¿ is presented.
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