These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: [Molecular mechanism of action of the fibrates]. Author: Fruchart JC, Duriez P, Staels B. Journal: J Soc Biol; 1999; 193(1):67-75. PubMed ID: 10851558. Abstract: Fibrates are old hypolipidemic drugs with pleitropic effects on lipid metabolism. Until, recently their intimate molecular mechanisms of action were mysterious. In the late 5 years, we have shown that the pharmacological effects of fibrates depend on their binding to "Peroxisome Proliferator Activated Receptor alpha" (PPAR alpha). The binding of fibrates to PPAR alpha induces the activation or the inhibition of multiple genes involved in lipid metabolism through the binding of the activated PPAR alpha to "Peroxisome Proliferator Response Element" (PPRE) located in the gene promoters. Fibrates reduce plasma triglyceride levels by altering the expression of numerous genes coding for proteins involved in fatty acid metabolism (fatty acid transport protein, acyl-CoA synthetase, etc.) and also by increasing the lipoprotein lipase synthesis and decreasing the apolipoprotein C-III synthesis. Fibrates increase HDL cholesterol levels by increasing apolipoprotein A-I and apolipoprotein A-II synthesis. Furthermore, we recently demonstrated that fibrates are potent anti-inflammatory molecules through an indirect modulation of the nuclear-factor-kappa B activity. Therefore, we suggest that fibrates inhibit atherosclerosis development not only by improving the plasma lipid profile but also by reducing inflammation in the vascular wall.[Abstract] [Full Text] [Related] [New Search]