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. 2021 Jul 1;15:690410. doi: 10.3389/fnins.2021.690410

FIGURE 2.

FIGURE 2

LT-krill oil treatment resulted in enriched plasma and brain levels of EPA in male and female APOE3-TR and APOE4-TR mice. (A) For plasma EPA levels, there was a treatment × APOE genotype × sex interaction [F(2, 48) = 5.89, p = 0.0051]. Plasma EPA levels followed the order LT-krill oil (15–34-fold) > krill oil (5–13-fold) > control within each genotype for a particular sex. APOE genotype and sex did not alter EPA levels in control diet groups; however, they did change the extent when plasma EPA was enriched with krill oil and LT-krill oil diets with EPA levels higher with APOE3 and female sex. (B) Plasma concentrations of LPC-EPA (nmol/ml plasma) were impacted by treatment [F(2, 30) = 808.8, p < 0.0001], genotype [F(1, 30) = 35.86, p < 0.0001], and treatment × APOE genotype interaction [F(2, 30) = 23.91, p < 0.0001] in female APOE3 and APOE4 mice. For both genotypes, LT-krill oil resulted in higher plasma LPC-EPA concentrations than krill oil (p < 0.0001) or control diets (p < 0.0001), and across all treatments, plasma LPC-EPA concentrations were lower in APOE4 than in APOE3 mice. The treatment × APOE genotype interaction was likely driven by a larger increase in plasma LPC-EPA concentrations with LT-krill oil treatment in APOE3 female mice (40-fold) compared with APOE4 female mice (36-fold). (C) Treatment, APOE genotype, and sex independently affected hippocampal EPA levels as the levels followed LT-krill oil > krill oil > control and were lower with APOE4 and female sex. All data expressed as mean ± SEM. *p < 0.05 by three-way ANOVA and Tukey’s post hoc analysis. #Different from APOE3 by Tukey’s post hoc analysis, p < 0.05. See Supplementary Table 1 for details on n sizes and statistical comparisons. C, control diet; K, krill oil diet; L, lipase-treated krill oil diet.