title: Apolipoprotein L-I is positively associated with hyperglycemia and plasma triglycerides in CAD patients with low HDL.
abstract: Apolipoprotein L-I (apoL-I) is present on a subset of HDL particles and is positively correlated with plasma triglycerides (TGs). We measured plasma apoL-I levels in coronary artery disease (CAD) subjects with low HDL who were enrolled in an angiographic CAD prevention trial. At baseline, apoL-I levels (n = 136; range, 2.2-64.1 mug/ml) were right skewed with a large degree of variability. Multivariate analysis for biological determinants of apoL-I revealed that the log of VLDL-TG (+0.17; P < 0.05) and hyperglycemia (HG; +0.26; P < 0.005) independently predicted apoL-I level. Hyperglycemic patients (n = 24) had mean apoL-I levels >50% higher than normoglycemic subjects (n = 112; 13.2 vs. 8.3 mug/ml, respectively; P < 0.001). No relationship between apoL-I level and change in CAD was found (r = 0.06, P = 0.49). Simvastatin-niacin therapy did not alter apoL-I levels (n = 34; P = 0.27), whereas antioxidant vitamins alone increased apoL-I by >50% (n = 36; P < 0.01). Genotyping of a known apoL-I polymorphism (Lys166Glu) did not independently account for any of the variability in apoL-I levels. In conclusion, we found TG and HG to be the strongest predictors of apoL-I within a dyslipidemic CAD population. These data provide further characterization of the novel HDL-associated apoL-I.
authors.affiliation: Department of Medicine, University of Washington, Seattle, WA, USA.
authors.forename: Timothy S E
authors.initials: TS
authors.lastname: Albert
authors.forename: Philippe N
authors.initials: PN
authors.lastname: Duchateau
authors.forename: Samir S
authors.initials: SS
authors.lastname: Deeb
authors.forename: Clive R
authors.initials: CR
authors.lastname: Pullinger
authors.forename: Min H
authors.initials: MH
authors.lastname: Cho
authors.forename: David C
authors.initials: DC
authors.lastname: Heilbron
authors.forename: Mary J
authors.initials: MJ
authors.lastname: Malloy
authors.forename: John P
authors.initials: JP
authors.lastname: Kane
authors.forename: B Greg
authors.initials: BG
authors.lastname: Brown
mesh_terms: D000368:Aged; D000975:Antioxidants / Q000494:pharmacology; D000075944:Apolipoprotein L1; D001053:Apolipoproteins / Q000097:blood* / Q000187:drug effects / Q000235:genetics; D003327:Coronary Disease / Q000097:blood*; D003430:Cross-Sectional Studies; D005260:Female; D014644:Genetic Variation; D005838:Genotype; D006801:Humans; D006943:Hyperglycemia / Q000097:blood*; D008075:Lipoproteins, HDL / Q000097:blood* / Q000187:drug effects / Q000235:genetics; D008297:Male; D008875:Middle Aged; D010919:Placebos; D012044:Regression Analysis; D014280:Triglycerides / Q000097:blood*
chemical_list: C108666:APOL1 protein, human; D000975:Antioxidants; D000075944:Apolipoprotein L1; D001053:Apolipoproteins; D008075:Lipoproteins, HDL; D010919:Placebos; D014280:Triglycerides