Peroxisome proliferator-activated receptor α (PPARα) activators induce hepatic farnesyl diphosphate synthase gene expression in rodents

Ginger phytochemicals mitigate the obesogenic effects of a high‐fat diet in mice: A proteomic and biomarker network analysis

“…FPPS is involved in the formation of farnesyl diphosphate from isopentyl diphosphate 30 and is an upstream enzyme in the biosynthesis of cholesterol 31. Gene expression of FPPS and other cholesterogenesis genes are regulated by sterol regulatory element‐binding proteins (SREBPs) 32 and the activation of SREBP is inhibited by the presence of sterols, such as cholesterol.…”

“…Fibrates are activators of the key transcription factor PPARα, which regulates fatty acid oxidation, increase HDL cholesterol and reduce plasma TGs 33. Fibrate influences on cholesterol metabolism are thought to be mediated by PPARα‐stimulated expression of FPPS through modulation of SREBP activation 31. Expression of the ACAA1 gene (alternatively known as peroxisomal 3‐ketoacyl CoA thiolase 1), is also directly regulated by PPARα and performs the fourth and final step in the peroxisomal β‐oxidation of fatty acids 34.…”

Farnesyl phosphates are endogenous ligands of lysophosphatidic acid receptors: Inhibition of LPA GPCR and activation of PPARs

“…Furthermore, activation of PPARα by fibrates induced FDP synthase gene expression in both hepatocytes and in mouse liver. This effect appears to be dependent on the cellular sterol level, possibly through sterol regulatory element binding protein (SREBP)-mediated transcriptional activation [25]. FDP synthase carries a 20-amino acid region that is required for the peroxisomal localization of the enzyme [26], which sets up a potential feed-forward loop between FMP/FDP and the regulation of peroxisomes.…”