Sialylated isoforms of apolipoprotein C-III and plasma lipids in subjects with coronary artery disease

Abstract

Abstract Background: Apolipoprotein C-III (ApoC-III), a key regulator of plasma triglyceride (TG), is present in three isoforms, i.e. non-sialylated (ApoC-III0), monosialylated (ApoC-III1) and disialylated (ApoC-III2). We aimed at quantifying the distribution of the ApoC-III glycoforms in patients with angiographically demonstrated coronary artery disease (CAD) according to levels of total ApoC-III plasma concentration. Methods: ApoC-III glycoforms were quantified by a specifically developed, high-resolution, mass spectrometry method in unrelated CAD patients. Lipoprotein lipase (LPL) activity was estimated by a fluorescence-based method. Results: In 101 statin-treated CAD patients, the absolute concentrations of the three glycoforms similarly increased across ApoC-III quartiles, but the proportion of ApoC-III1 rose whereas that of ApoC-III0 decreased progressively by increasing total ApoC-III concentrations. The proportion of ApoC-III2 was quite constant throughout the whole range of total ApoC-III. A higher proportion of ApoC-III1 reflected an unfavorable lipid profile characterized by high levels of TG, total and low density lipoprotein cholesterol, ApoE and reduced ApoA-I. The correlations between ApoC-III glycoforms and TG were confirmed in 50 statin-free CAD patients. High concentration of total ApoC-III was associated with low LPL activity, while no correlation was found for the relative proportion of glycoforms. Conclusions: Specific patterns of ApoC-III glycoforms are present across different total ApoC-III concentrations in CAD patients. The inhibitory effect of ApoC-III on LPL appears related to total ApoC-III concentration, but not to the relative proportion of ApoC-III glycoforms.