Capillary isotachophoresis study of lipoprotein network sensitive to apolipoprotein E phenotype. 2. ApoE and apoC-III relations in triglyceride clearance

The plasma (P), VLDL (V) triglyceride and apoB (B) clearance rates were measured both as ‘mass’ clearance (k1) and ‘within the particle’ clearance in three patient groups (E33, E23 and E34 phenotypes) at heparin-induced lipolysis in vivo. The lipid (C)- and apoE (E)-specific lipoprotein profiles both before and after heparin were followed by capillary isotachophoresis. The displacement of apoE by exogenous apoC-III at plasma titration in vitro was measured as well. The phenotype-sensitive lipoprotein networks were constructed based on an established set of metabolic rules. The k1(V) values did not differ between the three groups, but the lower k1(P) values showed significant differences. The k1(P) values for E33 and E23 groups were twofold higher compared to E34. A twofold increase in the rate constant for VLDL triglyceride clearance within the particle in E34 group compared to E23 reflected the inhibition of lipolysis by apoE2. For E33 group, (i) the k1(V) value was negatively correlated to the size of non-displaceable apoE pool in 2E lipoprotein and to the maximal apoE sorbtion capacity for 2E and 3E lipoproteins; (ii) the k1(P) value was not associated to the apoE binding parameters; (iii) the k1(V) value was positively correlated to the 4C level and the magnitude of apoC-III removal from VLDL particle; (iv) the k1(P) value was positively correlated to the content of apoE, while negatively with apoC-III, in VLDL remnants. For E34 group, the k1(V) value was positively correlated to 11C and 1–7C pool levels. Lipolysis- and receptor-mediated TG runways seem to be mostly balanced in E33 group, and VLDL TG clearance may be controlled by HDL through apoE dissociation from VLDLs and apolipoprotein accumulation within ‘fast’ HDLs at lipolysis.