Modeling the postprandial CETP-mediated lipid redistribution between chylomicrons, LDL and HDL

Figures

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  Fig. 1. Calculation of CM-associated components. g and f denote the concentration of a lipid or an polipoprotein in CMs or plasma without CMs (illustrated as exemplary chromatography), respectively, either before (b) or after (a) spin in the inner chamber (IC) or outer chamber (OC) of the liner. The dilution factors da,OC and da,IC are estimated for each sample via ApoA1 concentration.

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  Fig. 2. Concentrations of lipids and apolipoproteins at fasting state. Lipids total (A), apolipoproteins total (B), lipids from CM and IDL (C), lipids in VLDL + CMR, LDL, and HDL (D), ApoB-100 and ApoB-48 lipoprotein fractions and LDL subfractions (E), and ApoA1 in HDL, LDS, and HDL subfractions (F). Black circle with whiskers: quartiles of normolipidemics (n = 12), purple triangles: hypertriglyceridemics (n = 2), and red circles: hyperchylomicronemia (n = 2). LDS, lipid-deficient serum.

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  Fig. 3. Percentage change between fasting and postprandial (3–4 h after ingestion) state in lipids and apolipoproteins of the lipoprotein fractions VLDL, IDL, LDL + subfractions, HDL + subfractions (A), total plasma (B), CM (C), and calculated parameters, which are important for modeling redistribution of TG via CETP (D). Black circle with whiskers: quartiles of normolipidemics (n = 12) Wilcoxon signed-rank test, purple triangles: hypertriglyceridemics (n = 2).

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  Fig. 4. Summary: The effect of postprandial state on CETP-mediated TG-flux and lipoprotein fractions. CETP-mediated TG net fluxes at fasting (A) and postprandial state (B) in normolipidemics (n = 12). The surface of the circles (lipoprotein fractions), rectangles (ApoC3), and the thickness of the arrows are proportional to the surface of the fractions, the concentration of ApoC3 and the TG net flux, respectively. The proportion of TG/(CE + TG) and CE/(CE + TG) in the fractions is displayed blue and orange, respectively. The CETP-mediated TG net fluxes and the TG concentration of the fractions (blue) are displayed (A). The change in surface and the CE-TG proportion at postprandial state is displayed in (B) in gray. Changes in CM, VLDL, and LDL surface are significant. CMRs are included in the VLDL fraction.

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  Fig. 5. Lipoprotein composition (median) in fasting (A) and postprandial (B) state (wt/wt) in normolipidemics (solid) and hyperlipidemics (n = 2, dashed). Light blue = TG, orange = FC, gray = PL, dark blue = ApoB, yellow = ApoA1, and green = CE. Concentration (median and quartiles) of these components combined in fasting (white solid bars) and postprandial (gray solid bars) state (C) in normolipidemics (solid) (∗<0.05, ∗∗<0.01, Wilcoxon signed-rank test, n = 12) and hyperlipidemics (n = 2, fasting: black dashed bars, postprandial: gray solid bars).

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  Fig. 6. Comparison between observed = black and modeled (either “not discriminating model” = blue or “discriminating model” = green) TG net fluxes in LDL, IDL, and HDL per hour (circle with whiskers: quartiles of n = 12 normolipidemics, circles with purple border: hypertriglyceridemics [n = 2]). Fluxes were modeled in two ways: Using data, either in which CM and VLDL are merged (nondiscriminating model) or in which both fractions are used (discriminating model). Significant differences between both models in the normolipidemic case are displayed (Wilcoxon signed-rank test). Observed data are derived by subtracting TG in the corresponding fractions from samples stored either for 1 h at 37°C (before separation and measurement) or not.

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  Fig. 7. Concentration of ApoC3 (A) and ApoC2 (B) in total, CM, VLDL, and HDL at fasting (black) and postprandial state (blue) in normolipidemics (n = 12) and hyperlipidemics (n = 2, purple borders).

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  Supplemental Figure S1.

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  Supplemental Figure S2.