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- W2741492283 abstract "The regulation of lipid and carbohydratemetabolism is essential for maintaining the energybalance of the body and enables cells to perform vitalfunctions. Improper control of these metabolicpathways can result in serious health problems,such as obesity-associated ‘metabolic syndrome’orsyndrome X, which is typified by increased risk ofcoronary artery diseases (CAD), diabetes andrelated problems, such as hypertension andlipidemia. The recent demonstration of commondietary lipids and their metabolites as signalingmolecules for nuclear orphan receptors provides aunique approach to the study of metabolichomeostasis at the molecular level. These orphanreceptors are proposed to control lipid homeostasisby regulating of the expression of genetic networksinvolved in lipid metabolism, transport, storage andelimination [1]. Examples of such lipid sensorsinclude receptors for fatty acids [peroxisomeproliferator-activated receptors (PPARs)], oxysterols[liver X receptors (LXRs)], bile acids [farnesoidXreceptor (FXR)] and xenobiotics [pregnaneXreceptor (PXR), steroid xenobiotic receptor (SXR)and constitutive androstane receptor (CAR)].The PPARs comprise three subtypes [PPAR α,PPARδ(or β) and PPAR γ] with distinct expressionpatterns and biological functions [2,3]. Dietary fattyacids and arachidonate metabolites are naturalactivators of this receptor subfamily. PPAR αispredominantly expressed in liver, heart, muscle andkidney, where it regulates fatty acid catabolism [4].Consistent with this notion, the fibrate class oflipid-lowering drugs, such as fenofibrate (Controlip®)and gemfibrozil (Lopid®), were found to be syntheticactivators of PPAR α[5–7]. PPAR γis enriched inadipocytes and macrophages and can be activated bythe thiazolidinedione (TZD) chemical class ofantidiabetic drugs [8–10], including rosiglitazone(Avandia®) and pioglitazone (Actos®). Molecular andgenetic studies have established roles for PPAR γinadipocyte differentiation, lipid storage and glucosehomeostasis [11–13]. PPAR δis expressed in mosttissues and has a less defined function. It isimplicated in lipid homeostasis, keratinocyteproliferation and wound healing, and is a candidatefor drug development [14–16].Much attention has focused on the roles of PPAR γand the effects of its ligands in macrophage biologyfollowing the discovery that agonists of PPAR γpromote lipid accumulation whilst suppressingcytokine-induced macrophage activation [17–20].These original studies implicated PPAR γin bothproatherogenic and antiatherogenic(anti-inflammatory) pathways mediated bycomponents of oxidized-low density lipoprotein(ox-LDL) and 15-deoxy- ∆" @default.
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- W2741492283 date "2002-01-01" @default.
- W2741492283 modified "2023-09-27" @default.
- W2741492283 title "Peroxisome proliferator-activated receptor-γin macrophage lipid homeostasis" @default.
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