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* Lipid Metabolism Laboratory, Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA
Department of Internal Medicine and Molecular Science, Osaka University, Suita, Japan
Department of Medicine, University of Maryland, Baltimore, MD
** Center E Grossi Paoletti, Department of Pharmacological Sciences, University of Milan, Milan, Italy
Published, JLR Papers in Press, December 20, 2006.
1 To whom correspondence should be addressed. e-mail: bela.asztalos{at}tufts.edu
To better understand the role of LCAT in HDL metabolism, we compared HDL subpopulations in subjects with homozygous (n = 11) and heterozygous (n = 11) LCAT deficiency with controls (n = 22). Distribution and concentrations of apolipoprotein A-I (apoA-I)-, apoA-II-, apoA-IV-, apoC-I-, apoC-III-, and apoE-containing HDL subpopulations were assessed. Compared with controls, homozygotes and heterozygotes had lower LCAT masses (–77% and –13%), and LCAT activities (–99% and –39%), respectively. In homozygotes, the majority of apoA-I was found in small, disc-shaped, poorly lipidated preß-1 and 
-4 HDL particles, and some apoA-I was found in larger, lipid-poor, discoidal HDL particles with -mobility. No apoC-I-containing HDL was noted, and all apoA-II and apoC-III was detected in lipid-poor, preß-mobility particles. ApoE-containing particles were more disperse than normal. ApoA-IV-containing particles were normal. Heterozygotes had profiles similar to controls, except that apoC-III was found only in small HDL with preß-mobility. Our data are consistent with the concepts that LCAT activity: 1) is essential for developing large, spherical, apoA-I-containing HDL and for the formation of normal-sized apoC-I and apoC-III HDL; and 2) has little affect on the conversion of preß-1 into -4 HDL, only slight effects on apoE HDL, and no effect on apoA-IV HDL particles.
Supplementary key words HDL subpopulations • apolipoproteins • reverse cholesterol transport
Abbreviations: apoA-I, apolipoprotein A-I; CAD, coronary artery disease; CETP, cholesteryl ester transfer protein; EL, endothelial lipase; FC, free cholesterol; FED, fish eye disease; FLD, familial LCAT deficiency; HDL-C, HDL cholesterol; sPLA2, secretory phospholipase A2; SR-BI, scavenger receptor type B-I; TG, triglyceride
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