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Remnant Lipoproteins: Measurement and Clinical Significance

¹ University of Texas, Southwestern Medical Center, Dallas, TX 75390

^aAddress correspondence to this author at: UT Southwestern Medical Center, 5323 Harry Hines Blvd., CS3.114, Dallas, TX 75390-9073. Fax 214-648-8037; e-mail Jialal.i@pathology.swmed.edu.

In this issue of the Journal, Chan et al. (1) make the significant observation, by three distinct measures, that the concentrations of remnant lipoproteins (RLPs) in plasma are increased in patients with obesity. This increase in RLPs could explain, in part, the increased cardiovascular risk associated with obesity (2). To date, although LDL- and HDL-cholesterol are clearly accepted as independent risk factors for premature atherosclerosis, the role of plasma triglycerides as a risk factor remains somewhat controversial.

Plasma triglycerides are clearly a measure of triglyceride-rich lipoproteins (TRLs), which derive from both the intestine and the liver. Measurement of plasma triglycerides, however, does not distinguish the various subspecies of TRLs, which clearly have various degrees of atherogenicity. Triglyceride-rich RLPs are formed in the circulation when chylomicrons of intestinal origin [with apolipoprotein B-48 (apo B-48)] and VLDL of hepatic origin (with apo B-100) are converted by lipoprotein lipase (and to a lesser extent by hepatic lipase) into smaller and more dense particles. Compared with their nascent precursors, RLPs are depleted of triglycerides, phospholipids, and apo C and are enriched in cholesteryl esters and apo E and are believed to be more atherogenic than the larger TRLs (3).

Several lines of evidence have implicated RLPs in premature atherosclerosis. In fact, the prototypic disorder of remnant metabolism, type III dyslipidemia, is associated with accelerated atherosclerosis (4). Other evidence incriminating remnants as proatherogenic factors include the following: increased intermediate-density lipoprotein (IDL) concentrations have been associated with an increased incidence or recurrence of coronary artery disease (CAD) (3). Increased IDL is also found in diseases associated with accelerated atherosclerosis, such as type III dyslipidemia, type 2 diabetes mellitus, end stage renal disease (ESRD), and familial combined hyperlipidemia. Several previous reports have linked various measures of remnants . . . [Full Text of this Article]

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