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Effect of Two Common Polymorphisms in the ATP Binding Cassette Transporter A1 Gene on HDL-Cholesterol Concentration

Department of Laboratory Medicine and Pathology, University of Minnesota Medical School, Minneapolis, MN 55455

^aaddress correspondence to this author at: 420 Delaware Street SE, Mayo Mail Code 609, Minneapolis, MN 55455-0392; fax 612-625-5622, e-mail tsaix001@tc.umn.edu

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HDL-cholesterol (HDL-C) has long been recognized as having an atheroprotective role (1). Epidemiologic studies have shown that decreased HDL-C concentrations are the most common lipid abnormality in patients with premature coronary artery disease (CAD). Thus, there has been increased recognition of the inverse relationship between HDL-C concentrations and risk for CAD (2)(3). This heightened awareness is underscored by changes in the recommendations of the Adult Treatment Panel (ATP) of the National Cholesterol Education Program. For example, ATP II, published in 1993, first introduced the concept of a low HDL-C [<0.91 mmol/L (<35 mg/dL)] as a risk factor for CAD (4). More recently, ATP III further revised the cutoff for HDL-C as a risk factor to <1.04 mmol/L (<40 mg/dL) (5).

HDL-C is the primary lipoprotein particle responsible for reverse cholesterol transport (RCT) (6). RCT involves the transport of cholesterol from nonhepatic cells to the liver and its subsequent elimination from the body as bile acid and free cholesterol. A major advance in the understanding of RCT was heralded by the discovery of the gene encoding for ATP binding cassette transporter A1 (ABCA1). ABCA1, a member of the ABC transporter family, facilitates the active transport of cholesterol and phospholipids from the intracellular compartments of peripheral cells to the lipid-poor nascent HDL particle (7), thus representing the first step of the RCT pathway.

Deleterious mutations, when present in both alleles in the ABCA1 gene, were identified as the molecular basis for patients with Tangier disease, a disorder characterized by an almost complete absence of plasma HDL-C and an increased risk for CAD (8)(9)(10). Studies from our own laboratory, however, demonstrated that these detrimental mutations of the ABCA1 gene are probably not highly . . . [Full Text of this Article]