(15d-PGJ2) was the first endogenous PPARγ ligand identified45, 46. This prostaglandin is currently widely utilized as a naturally occurring PPARγ activator. Further, lipoxygenase metabolites 12-and 15-hydroxyeicosatetraenoic acid (HETE) are potent activators of PPARγ and are produced by interleukin 4 treated macrophages47. In addition, the insulin-sensitizing antidiabetic thiazolidinediones (TZD) bind and activate PPARγ. One such compound, rosiglitazone (BRL 49653) binds with a high affinity to PPARγ45, 48. All TZD tested to date, ie, BRL 49653, pioglitazone, and troglitazone, bind and activate the PPARγ isotype with Kd that parallel their antidiabetic activity in vivo45, 48-50. In addition to TZD, other synthetic compounds have been identified as PPARγ activators. It has been shown that several NSAID, such as indomethacin, ibuprofen, fenoprofen, and flufenamic acid, bind and activate PPARγ and promote adipocyte differentiation41, 51, 52. In contrast to the other subtypes, no selective drugs to PPARß/δ have been identified so far. Many natural and synthetic compounds have been shown to bind and activate PPARß/δ, in particular polyunsaturated fatty acids37, 40 and the semisynthetic PGI analog carbaprostacyclin37. Lastly, the eicosanoid PGA1 preferentially activates this subtype, suggesting that endogenous PPARß/δ ligands are derived from the cyclooxygenase (COX) pathway37, 38. More information relating to the structure of PPAR, their putative ligands, and their many biological activities can be found in recent reviews42, 53, 54.