 Recently, it has been recognized that circulating levels of Triglyceride and HDL-C are influenced by the activities of Peroxisome Proliferator Activator Receptors PPARs. PPARs constitute a super family of nuclear hormone receptors and are ligand-activated transcription factors. When activated, they transmit signals from intra-cellular lipid-soluble factors e.g. fatty acids, hormones, vitamins to genes in the nucleus by binding to DNA at specific response elements 13. Three distinct PPARs, termed alpha, beta, and gamma modulate intracellular lipid and glucose metabolism through controlling gene expression when activated 14. Specifically when PPAR-alpha is activated, gene expression for the synthesis of ApoC-III, lipoprotein lipase, ApoA-I and ApoA-II are impacted. ApoC-III is a specific inhibitor of peripheral lipoprotein lipase and competes with ApoE for space on the surface of VLDL. Reduced amounts of ApoC-III will result in a larger representation of ApoE on the VLDL particle, and as a consequence, the ApoE mediated hydrolysis of Triglycerides is enhanced. Activation of PPAR-alpha leads to decrease production of ApoC-III, which in turn results in enhanced clearance of Triglycerides. Activation of PPAR-alpha also increases the synthesis of lipoprotein lipase, which increases Triglyceride catabolism. Gene expression for the synthesis of ApoA-I and ApoA-II is also enhanced by activation of PPAR-alpha, resulting in increase in HDL concentration. Fibric acid derivatives Gemfibrozil and Fenofibrate induce their Triglyceride lowering and HDL-C augmenting properties by binding to the PPAR-alpha nuclear receptor. 