title: Plasma apolipoprotein L concentrations correlate with plasma triglycerides and cholesterol levels in normolipidemic, hyperlipidemic, and diabetic subjects.
abstract: Apolipoprotein L is a newly recognized component of human plasma lipoproteins. Mainly associated with apoA-I-containing lipoproteins, it is a marker of distinct HDL subpopulations. In an effort to gain inference as to its as yet unknown function, we studied biological determinants of apoL levels in human plasma. The distribution of apoL in normal subjects is asymmetric, with marked skewing toward higher values. No difference was found in apoL concentrations between males and females, but we observed an elevation of apoL in primary hypercholesterolemia (10.1 vs. 8.5 microgram/mL in control), in endogenous hypertriglyceridemia (13.8 microgram/mL, P < 0.001), combined hyperlipidemia phenotype (18.7 g/mL, P < 0.0001), and in patients with type II diabetes (16.2 microgram/mL, P < 0.02) who were hyperlipidemic. Significant positive correlations were observed between apoL and the log of plasma triglycerides in normolipidemia (0.446, P < 0.0001), endogenous hypertriglyceridemia (0.435, P < 0.01), primary hypercholesterolemia (0.66, P < 0.02), combined hyperlipidemia (0.396, P < 0.04), hypo-alphalipoproteinemia (0.701, P < 0.005), and type II diabetes with hyperlipidemia (0.602, P < 0. 01). Apolipoprotein L levels were also correlated with total cholesterol in normolipidemia (0.257, P < 0.004), endogenous hypertriglyceridemia (0.446, P = 0.001), and non-insulin-dependent diabetes mellitus (NIDDM) (0.548, P < 0.02). No significant correlation was found between apoL and body mass index, age, sex, HDL-cholesterol or fasting glucose and glycohemoglobin levels. ApoL levels in plasma of patients with primary cholesteryl ester transfer protein deficiency significantly increased (7.1 +/- 0.5 vs. 5.47 +/- 0.27, P < 0.006).
authors.affiliation: Cardiovascular Research Institute, University of California, San Francisco, CA 94143, USA.
authors.forename: P N
authors.initials: PN
authors.lastname: Duchateau
authors.forename: I
authors.initials: I
authors.lastname: Movsesyan
authors.forename: S
authors.initials: S
authors.lastname: Yamashita
authors.forename: N
authors.initials: N
authors.lastname: Sakai
authors.forename: K
authors.initials: K
authors.lastname: Hirano
authors.forename: S A
authors.initials: SA
authors.lastname: Schoenhaus
authors.forename: P M
authors.initials: PM
authors.lastname: O'Connor-Kearns
authors.forename: S J
authors.initials: SJ
authors.lastname: Spencer
authors.forename: R B
authors.initials: RB
authors.lastname: Jaffe
authors.forename: R F
authors.initials: RF
authors.lastname: Redberg
authors.forename: B Y
authors.initials: BY
authors.lastname: Ishida
authors.forename: Y
authors.initials: Y
authors.lastname: Matsuzawa
authors.forename: J P
authors.initials: JP
authors.lastname: Kane
authors.forename: M J
authors.initials: MJ
authors.lastname: Malloy
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000075944:Apolipoprotein L1; D001053:Apolipoproteins / Q000097:blood*; D002352:Carrier Proteins / Q000235:genetics; D002784:Cholesterol / Q000097:blood*; D053480:Cholesterol Ester Transfer Proteins; D003924:Diabetes Mellitus, Type 2 / Q000097:blood*; D005260:Female; D006023:Glycoproteins; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood; D006949:Hyperlipidemias / Q000097:blood*; D015228:Hypertriglyceridemia / Q000097:blood; D008075:Lipoproteins, HDL / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009154:Mutation; D013631:Tangier Disease / Q000097:blood; D014280:Triglycerides / Q000097:blood*
chemical_list: C108666:APOL1 protein, human; D000075944:Apolipoprotein L1; D001053:Apolipoproteins; C506642:CETP protein, human; D002352:Carrier Proteins; D053480:Cholesterol Ester Transfer Proteins; D006023:Glycoproteins; D008075:Lipoproteins, HDL; D014280:Triglycerides; D002784:Cholesterol