Fig 1: Impact of the intake of ω3-milk on the high density lipoprotein (HDL) profile. Box-Plots and 2-DE representative images showing the significant changes induced in HDL proteins by ω3-milk: (a) Apo A–I (p = 0.009); (b) lecitin cholesterol acyltransferase (LCAT) (p = 0.044); (c) paraoxonase-1 (PON-1) (p = 0.047); (d) Apo D (p = 0.008); and (e) Apo L1 (p = 0.038).
Fig 2: Changes on lecitin cholesterol acyltransferase (LCAT) serum levels after ω3-milk intake. Box-Plot diagrams showing LCAT concentration (µg/mL) in basal conditions and after the intake of ω3-milk, measured by a commercial ELISA. (a) No change was observed when all the volunteers were analyzed (N = 32; p = 0.346). (b) There was a significant increase in LCAT serum levels in subjects that showed a reduction in TG levels after ω3-milk intake (N = 11; p = 0.0397).
Fig 3: Simplified diagram of the lipid metabolism canonical pathway. Maturation of HDL and free cholesterol (FC) esterification are catalyzed by LCAT. Apo A-I and Apo E activate LCAT, and PON-I, which is also activated by Apo A–I, avoiding LCAT inactivation. Apo D binds to LCAT to improve its esterification activity. Finally, cholesterol is transported to the liver for its elimination by fecal excretion.
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