Mode of action of fibrates in the regulation of @entity412 and HDL- XXXX metabolism.

@entity2298 @entity12436 @entity3724 @entity844 @entity301 @entity731 @entity1674 @entity49032 @entity412 @entity1675 @entity5601 @entity10569 @entity453 @entity3294 @entity1718 @entity30821 @entity8445 @entity165
Epidemiological studies have shown that @entity2298 and low HDL- @entity165 were both associated with an increased risk of @entity301 . Furthermore, @entity2298 is now recognized as an independent risk factor for @entity453 . Secondary prevention trials (e.g., LOCAT, BECAIT, @entity30821 and DAIS) in @entity453 with drugs acting primarily on @entity1674 (e.g., the @entity5601 activators @entity10569 , @entity3724 and @entity8445 ) have shown that reducing @entity1674 and increasing HDL- @entity165 , without significantly affecting LDL- @entity165 , slows down coronary artery luminal narrowing. Furthermore, the VA-HIT study recently showed that @entity8445 decreased @entity453 mortality in secondary prevention trials, partly by increasing HDL- @entity165 . The peroxisome proliferator-activated receptors (PPARs) (i.e., @entity49032 ) form a subfamily of the nuclear receptor gene family. Whereas all PPARs are, albeit to differing extents, activated by @entity1718 and derivatives, @entity5601 binds the hypolipidemic fibrates. @entity5601 activation mediates changes in lipoprotein metabolism. Moreover, @entity5601 activators increase hepatic uptake and esterification of free @entity1718 , in addition to increasing mitochondrial free @entity844 uptake and the resulting free @entity844 oxidation. The effect of fibrates on the metabolism of @entity412 -rich lipoproteins is due to a @entity5601 -dependent stimulation of lipoprotein lipase and of apolipoprotein (apo)A-V and to an inhibition of @entity12436 expression, whereas the increase in plasma HDL- @entity165 depends partly on an overexpression of @entity1675 and @entity3294 . PPARs are also expressed in @entity731 .
