• PPARα gene
• Val227Ala polymorphism
• serum lipid levels

Peroxisome proliferator activated receptors (PPARs) are ligand activated transcription factors that belong to the nuclear receptor superfamily.^{1, 2} PPARs regulate gene transcription by heterodimerising with retinoic X receptors and binding to DNA sequences, termed PPAR response elements (PPRE), in the promoters of target genes.^{2, 3}

Three different PPAR genes (α, δ/β, and γ), each displaying distinct tissue and developmental expression patterns, have been identified.^{4, 5}PPARα, the first member of the PPAR family to be identified, was cloned as an orphan receptor activated by agents that induce peroxisome proliferation.⁶ It is expressed primarily in tissues with high levels of fatty acid oxidation, such as those in liver, kidney, heart, and muscle.^{4, 6} Most target genes of PPARα encode enzymes involved in oxidation of cellular fatty acids, lipid transporters, and apolipoproteins.^{1, 7} Furthermore, PPARα is known to mediate the actions of fibrates, which are hypolipidaemic drugs that decrease plasma triglycerides and increase high density lipoprotein (HDL) cholesterol concentrations.^{8, 9} Numerous in vivo and in vitro studies have suggested that PPARα is a key metabolic regulator involved in lipid and glucose homeostasis.^{1, 10–12} Recently, a Leu162Val polymorphism was identified in the PPARα gene, and this polymorphism was shown to influence plasma lipid concentrations, especially in type II diabetes patients.^{13, 14} In the present study, we have screened for polymorphisms in the PPARα gene to determine whether genomic variations in this gene influence serum lipid levels, glucose levels, and body mass index (BMI) in healthy subjects.