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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:2013.)
© 2005 American Heart Association, Inc.

Editorials

Fat, Fit, and Leading the Charge

The Evolution of Measuring High-Density Lipoprotein Subpopulations

Vijay Nambi; Christie M. Ballantyne

From the Sections of Cardiology (V.N.) and Atherosclerosis and Lipoprotein Research (C.M.B.), Department of Medicine, Baylor College of Medicine, and the Center for Cardiovascular Disease Prevention (C.M.B.), Methodist DeBakey Heart Center and Baylor College of Medicine; Houston, Texas.

Correspondence to Christie M. Ballantyne, Baylor College of Medicine 6565 Fannin, M.S. A-601 Houston, TX 77030. E-mail cmb@bcm.tmc.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Reduced plasma levels of high-density lipoproteins (HDL) were found to be associated with increased risk of atherosclerosis more than 50 years ago. Diverse methodologies including electrophoresis, ultracentrifugation, and biochemical characterization were used even at that time to examine the association between the cholesterol, phospholipid, and protein composition of HDL, also known as -lipoproteins, and atherosclerosis.^1–4 Within 25 years of these seminal observations, the model was proposed in which atherosclerosis is driven by an excess of atherogenic lipoproteins (primarily low-density lipoprotein), which are deposited in the vessel wall, and a deficiency of protective HDL particles, which control cholesterol efflux from the vessel wall.⁵

See page 2185

In our current models of atherosclerosis, the major mechanism for the atheroprotective properties of HDL is thought to be reverse cholesterol transport, a process by which lipid-poor nascent HDL particles accept cholesterol from peripheral cells through the interaction of apolipoprotein A-I (apoA-I), the major protein of HDL, with ATP-binding cassette protein A1. After esterification of the cholesterol by the interaction of lecithin:cholesterol acyltransferase and apoA-I, the HDL particle transfers the cholesteryl esters to the liver via scavenger receptor B1 or to the apoB-containing particles (in exchange for triglycerides) through the action of cholesteryl ester transfer protein.

The cholesterol content in HDL (HDL-C) has been inversely related to risk for coronary heart disease (CHD) in numerous epidemiological studies, with each 1-mg/dL increase in HDL-C associated with an 2% to 3% decrease in risk for CHD.⁶ Measurement of HDL-C is recommended for all adults to assess the . . . [Full Text of this Article]

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