title: Isolation and characterization of an apoA-II-containing lipoprotein (LP-A-II:B complex) from plasma very low density lipoproteins of patients with Tangier disease and type V hyperlipoproteinemia.
abstract: Previous studies have shown that very low density lipoproteins (VLDL) from patients with Tangier disease are less effective as a substrate for human milk lipoprotein lipase (LPL) than VLDL from normal controls as assessed by measuring the first order rate constant (k1) of triglyceride hydrolysis. Tangier VLDL also has a higher content of apolipoprotein (apo) A-II than normal VLDL. To explore the possible relationship between the relatively high concentration of apoA-II in VLDL and low k1 values, Tangier VLDL were fractionated on an anti-apoA-II immunosorber. The retained fraction contained a newly identified triglyceride-rich lipoprotein characterized by the presence of apolipoproteins A-II, B, C-I, C-II, C-III, D, and E (LP-A-II:B:C:D:E or LP-A-II:B complex), whereas the unretained fraction consisted of previously identified triglyceride-rich apoB-containing lipoproteins free of apoA-II. In VLDL from patients with Tangier disease or type V hyperlipoproteinemia, the LP-A-II:B complex accounted for 70-90% and 25-70% of the total apoB content, respectively. The LP-A-II:B complexes had similar lipid and apolipoprotein composition; they were poor substrates for LPL as indicated by their low k1 values (0.014-0.016 min-1). In contrast, the apoA-II-free lipoproteins present in unretained fractions were effective substrates for LPL with k1 values equal to or greater than 0.0313 min-1. These results indicate that triglyceride-rich lipoproteins consist of several apoB-containing lipoproteins, including the LP-A-II:B complex, and that lipoprotein particles of similar size and density but distinct apolipoprotein composition also possess distinct metabolic properties.
authors.affiliation: Lipoprotein and Atherosclerosis Research Program, Oklahoma Medical Research Foundation, Oklahoma City.
authors.forename: P
authors.initials: P
authors.lastname: Alaupovic
authors.forename: C
authors.initials: C
authors.lastname: Knight-Gibson
authors.forename: C S
authors.initials: CS
authors.lastname: Wang
authors.forename: D
authors.initials: D
authors.lastname: Downs
authors.forename: E
authors.initials: E
authors.lastname: Koren
authors.forename: H B
authors.initials: HB
authors.lastname: Brewer
authors.forename: R E
authors.initials: RE
authors.lastname: Gregg
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal; D016633:Apolipoprotein A-II; D001054:Apolipoproteins A / Q000097:blood*; D002846:Chromatography, Affinity; D004591:Electrophoresis, Polyacrylamide Gel; D005260:Female; D006801:Humans; D006954:Hyperlipoproteinemia Type V / Q000097:blood*; D015151:Immunoblotting; D008079:Lipoproteins, VLDL / Q000097:blood / Q000737:chemistry; D008297:Male; D008875:Middle Aged; D013631:Tangier Disease / Q000097:blood*; D014280:Triglycerides / Q000097:blood
chemical_list: D000911:Antibodies, Monoclonal; D016633:Apolipoprotein A-II; D001054:Apolipoproteins A; D008079:Lipoproteins, VLDL; D014280:Triglycerides