PPAR-α is a fatty acid-activated member of the PPAR subfamily of the nuclear receptor superfamily of transcription factors. Collectively the PPAR subfamily plays important roles in lipid and glucose metabolism, and has been implicated in obesity-related metabolic diseases such as hyperlipidemia, insulin resistance, and coronary artery disease. PPAR-α is expressed primarily in metabolic tissues (brown adipose tissue, liver, kidney) but elevated levels are also present in the digestive (jejunum, ileum, colon, gall bladder) and cardiopulmonary (aorta, heart) systems. PPAR-α dysfunction is associated with susceptibility to hyperapobetalipoproteinemia in addition to a variety of cardiovascular (myocardial infarction, ischemic heart disease, atherosclerosis, hypertension), immune (psoriasis), metabolic (plasma lipid levels, type II diabetes, body mass, plasma triglycerides and cholesterol, liver steatosis and steatohepatitis, hyperlipidemia, obesity, arterial blood pressure) and neurological (Alzheimer's disease) conditions. Targeted disruption (knockout) of the PPAR-α gene is associated with defects in adipose tissue, the cardiovascular system, growth and size, homeostasis and metabolism, the immune system, life span, the liver and biliary system, muscle and skin wound healing.