2006
DOI: 10.1097/01.med.0000216965.36504.be
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Different actions of peroxisome proliferator-activated receptors: molecular mechanisms and clinical importance

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Cited by 5 publications
(3 citation statements)
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“…PPARγ agonists such as thiazolidinedione rosiglitazone improve insulin resistance in patients with type 2 diabetes by modifying adipocyte differentiation. 39) Several groups using reporter gene and receptor binding assays demonstrated that MEHP activates PPARγ. [36][37][38] In addition to being metabolized through hydrolysis, PEs can be produced ring-or alkyl chainhydroxylated metabolites.…”
Section: Ppar-mediated Effects Of Hydroxylated Phthalate Estersmentioning
confidence: 99%
“…PPARγ agonists such as thiazolidinedione rosiglitazone improve insulin resistance in patients with type 2 diabetes by modifying adipocyte differentiation. 39) Several groups using reporter gene and receptor binding assays demonstrated that MEHP activates PPARγ. [36][37][38] In addition to being metabolized through hydrolysis, PEs can be produced ring-or alkyl chainhydroxylated metabolites.…”
Section: Ppar-mediated Effects Of Hydroxylated Phthalate Estersmentioning
confidence: 99%
“…PPAR are expressed in the liver, in the brown adipose tissue, in endothelial cells and vascular smooth muscle cells and their agonists are represented by fibrates, currently used in treatment of abnormalites in Tg and HDL; fibrates modestly affect low density lipoproteins (LDL) concentration, but have been shown to increase the percentage of larger, less atherogenic particles [7]. PPAR are mainly expressed in the adipose tissue, and, at low levels, in the liver and the vascular tissue.…”
Section: Peroxisome Proliferators Activated Receptors and Thiazolidinmentioning
confidence: 99%
“…To date, the thiazolidinediones approved for treatment of type 2 diabetes are pioglitazone (ActosTakeda Pharmaceuticals North America, Inc., Lincolnshire) and rosiglitazone (Avandia, Glaxo Smith Kline, research Triangle Park NC), while troglitazone has been withdrawn in 2000 because of many cases of hepatic toxicity. Thiazolidinediones were initially introduced as new insulin-sensitizers for the treatment of type 2 diabetes; subsequently, experimental and clinical studies results have clearly demonstrated a role of these molecules in the regulation of plasmatic lipids and adipose tissue endocrinological functions [7][8][9]. Thiazolidinediones have been shown to increase glucose disposal in skeletal muscle, thus leading to enhanced insulin-receptor signalling and concomitant reduction in plasma FFA [10].…”
Section: Peroxisome Proliferators Activated Receptors and Thiazolidinmentioning
confidence: 99%