Skip to main content
. 2025 Aug 28;5(1):100774. doi: 10.1016/j.gastha.2025.100774

Figure 2.

Figure 2

Arachidonic acid, linoleic acid, and LXR agonist exposure facilitate VLDL secretion in HLC. (A) Schematic overview of the AALAT protocol and lipoprotein separation using iodixanol gradient ultracentrifugation. The bar graph shows the effect of AALA and T0901317 treatments on the amount of VLDL in Fraction 1 (∗P < .05; Tukey’s post hoc tests). (B) Upper: Lipoproteins were isolated from the culture supernatants of control HLCs, AALAT-HLCs, and HepG2 cells, and ApoB100 levels were measured by ELISA (n = 3 per a group; ∗P < .05; Student’s t-test). Lower: The ratio of triglyceride to ApoB in each fraction from human plasma is shown (n = 6 per group). (C) ApoB100 secretion of control HLCs, AALAT HLCs and PHH was analyzed (∗∗∗P < .001, Tukey’s post hoc tests). (D) Hierarchical clustering was performed for the ratio of fatty acid content in PC of control HLC, AALAT HLC and human liver tissue. (E) The TG content of control HLCs and AALAT HLCs was analyzed (∗∗∗P < .001, Student’s t-test). (F) Gene expression levels related to lipoprotein assembly and de novo lipogenesis were measured by qRT-PCR in control-, AALA-, and AALAT-HLCs. All data represent mean ± SD.