出版社：American Society for Biochemistry and Molecular Biology
摘要：To better understand the role of LCAT in HDL metabolism, wecompared HDL subpopulations in subjects with homozygous (n =11) and heterozygous (n = 11) LCAT deficiency with controls(n = 22). Distribution and concentrations of apolipoproteinA-I (apoA-I)-, apoA-II-, apoA-IV-, apoC-I-, apoC-III-, and apoE-containingHDL subpopulations were assessed. Compared with controls, homozygotesand 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, andsome apoA-I was found in larger, lipid-poor, discoidal HDL particleswith -mobility. No apoC-I-containing HDL was noted, and allapoA-II and apoC-III was detected in lipid-poor, preß-mobilityparticles. ApoE-containing particles were more disperse thannormal. ApoA-IV-containing particles were normal. Heterozygoteshad profiles similar to controls, except that apoC-III was foundonly in small HDL with preß-mobility. Our data areconsistent with the concepts that LCAT activity: 1) is essentialfor developing large, spherical, apoA-I-containing HDL and forthe 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-IVHDL 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
-4 HDL particles, and some apoA-I was found in larger, lipid-poor, discoidal HDL particles with 
