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HDL biology

Apolipoprotein L levels rise in primary CETP deficiency and correlate with triglycerides across hyperlipidemic and diabetic subjects (J Lipid Res 2000)

Original title: Plasma apolipoprotein L concentrations correlate with plasma triglycerides and cholesterol levels in normolipidemic, hyperlipidemic, and diabetic subjects

J Lipid Res · · 5

Duchateau PN, Movsesyan I, Yamashita S, Sakai N, Hirano K, Schoenhaus SA, O'Connor-Kearns PM, Spencer SJ, Jaffe RB, Redberg RF, Ishida BY, Matsuzawa Y et al.

Apolipoprotein L (apoL) is a newly recognized component of human plasma lipoproteins, mainly associated with apoA-I-containing particles and marking distinct HDL subpopulations. Its distribution in normal subjects was skewed toward higher values, with no difference between males and females. ApoL was elevated in primary hypercholesterolemia (10.1 vs. 8.5 microgram/mL in controls), endogenous hypertriglyceridemia (13.8 microgram/mL, P < 0.001), combined hyperlipidemia (P < 0.0001), and hyperlipidemic type II diabetes (16.2 microgram/mL, P < 0.02), and correlated positively with plasma triglycerides in most of these groups but not with body mass index, age, sex, HDL cholesterol, or glucose measures. ApoL levels were also significantly higher in patients with primary CETP deficiency than in controls (7.1 +/- 0.5 vs. 5.47 +/- 0.27, P < 0.006).

PubMed

Original 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).

HDL biology

Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 19 August 2026. Methods.