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Peroxisome proliferator activated receptors alpha (PPAR α ) and delta (PPAR δ ) belong to the nuclear receptor superfamily. PPAR α  is a target of well established lipid-lowering drugs. PPAR δ  (also known as PPAR β / δ ) has been investigated as a promising antidiabetic drug target; however, the evidence in the literature on PPAR δ  effect on hepatic lipid metabolism is inconsistent. Mice conditionally expressing human PPAR δ  demonstrated pronounced weight loss and promoted hepatic steatosis when treated with GW501516 (PPAR δ -agonist) when compared to wild type mice. This effect was completely absent in mice with either a dominant negative form of PPAR δ  or deletion of the DNA binding domain of PPAR δ . This confirmed the absolute requirement for PPAR δ  in the physiological actions of GW501516 and confirmed the potential utility against the human form of this receptor. Surprisingly the genetic deletion of PPAR α  also abrogated the effect of GW501516 in terms of both weight loss and hepatic lipid accumulation. Also the levels of the PPAR α  endogenous agonist 16:0/18:1-GPC were shown to be modulated by PPAR δ  in wild type mice. Our results show that both PPAR δ  and PPAR α  receptors are essential for GW501516-driven adipose tissue reduction and subsequently hepatic steatosis, with PPAR α  working downstream of PPAR δ .

PPARαIs Required for PPARδAction in Regulation of Body Weight and Hepatic Steatosis in Mice