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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:1201.)
© 2006 American Heart Association, Inc.

Editorials

Lipoprotein Metabolism

A Well-Tried Tool to Characterize Dyslipidemic Mechanisms

Lars Berglund

From the Department of Medicine, University of California, Davis, and the VA Northern California Health Care System, Sacramento, Calif.

Correspondence to Lars Berglund, MD, Department of Medicine, University of California Davis, UCD Medical Center, CRISP, 2921 Stockton Blvd Street, Suite 1400, Sacramento, CA 95817. E-mail lars. berglund@ucdmc.ucdavis.edu

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

Metabolic studies of lipoproteins have yielded important insights into regulation of energy distribution as well as providing fundamental understanding of cardiovascular risk properties of different lipoproteins. Although many factors on the molecular level have the potential to impact metabolic regulation of lipids, metabolic studies provide valuable information from a comprehensive regulatory viewpoint. With increasing emphasis on lipoprotein subfractions and their roles in promoting or protecting from cardiovascular risk, the focus of metabolic studies is largely moving toward more detailed understanding of lipoprotein subclass and individual apolipoprotein properties.

See page 1370

The atherogenic and antiatherogenic roles of LDL and HDL cholesterol, respectively, are well established and, by now, part of the general public knowledge. However, hereditary diseases of lipoprotein metabolism with dramatically different LDL and/or HDL cholesterol levels offer great promise to further investigate this complex system, and we have already gained considerable insight from such studies. Thus, it is well known that some hereditary conditions result in phenotypes with unusual LDL and HDL compositions. Thus, carriers of apoA-I Milano appear protected from cardiovascular disease in spite of low HDL cholesterol levels.^1,2 In another hereditary condition, lecithin:cholesterol acyltransferase (LCAT) deficiency, HDL metabolism is severely affected, and carriers of this deficiency have low levels of both HDL and LDL cholesterol with the accumulation of an aberrant lipoprotein, Lp-X.^3,4 However, in spite of low HDL cholesterol levels, cardiovascular disease is not common among LCAT-deficient subjects.^5,6 LCAT is critical for esterification of cholesterol, and in the absence of this enzyme HDL maturation is affected, . . . [Full Text of this Article]

Related Article:

Human Lecithin:Cholesterol Acyltransferase Deficiency: In Vivo Kinetics of Low-Density Lipoprotein and Lipoprotein-X

Masato Nishiwaki, Katsunori Ikewaki, Giovanni Bader, Hassan Nazih, Minna Hannuksela, Alan T. Remaley, Robert D. Shamburek, and H. Bryan Brewer, Jr
Arterioscler Thromb Vasc Biol 2006 26: 1370-1375. [Abstract] [Full Text] [PDF]