Fig 2: Hepatic LPL overexpression improves glucose metabolism and insulin resistance in HFD-fed mice.Male C57BL/6 mice were intravenously treated with Ad vectors via the tail vein and were simultaneously fed HFD. PBS-treated mice were fed ND throughout the experimental period. (A) Blood glucose levels during the intra-peritoneal glucose tolerance test of mice 2 weeks after administration of Ad-LPL, Ad-Luc, or PBS. (B) Fasting blood glucose levels of mice 1 and 2 weeks after administration of Ad-LPL, Ad-Luc, or PBS. (C) Blood glucose levels during the intra-peritoneal insulin tolerance test of mice 2 weeks after administration of Ad-LPL, Ad-Luc, or PBS. (D) Fasting insulin levels and (E) HOMA-IR of mice 2 weeks after administration of Ad-LPL, Ad-Luc, or PBS. One-way ANOVA with Dunnett’s post hoc tests was used for multiple comparisons (A, B, D, and E). The Mann–Whitney U test was used to compare differences between two independent groups (C). The data are expressed as the mean ± standard error (n = 4–5). *, P < 0.05 in comparison with Ad-Luc.

Fig 3: Hepatic LPL overexpression upregulates fatty acid oxidation-related genes and protein in HFD-fed mice.Male C57BL/6 mice were intravenously treated with Ad vectors via the tail vein and were simultaneously fed HFD. PBS-treated mice were fed ND throughout the experimental period. Hepatic (A) PPARa, (B) CPT1, and (D) ACOX1 mRNA levels in male C57BL/6 mice 2 weeks after administration of Ad-LPL, Ad-Luc, or PBS determined using quantitative RT-PCR. The data were normalized to the corresponding value in the Ad-Luc-treated group. One-way ANOVA with Dunnett’s post hoc tests was used for multiple comparisons. The data are expressed as the mean ± standard error (n = 5). Hepatic (C) CPT1 and (E) ACOX1 protein levels in male C57BL/6 mice 2 weeks after administration of Ad-LPL or Ad-Luc determined using western blot analysis. The quantification data were normalized to the corresponding value in the Ad-Luc-treated group. The Mann–Whitney U test was used to compare the differences between two independent groups. The data are expressed as the mean ± standard error (n = 3). *, P < 0.05 vs. Ad-Luc.

Fig 4: Hepatic LPL overexpression maintains mitochondrial content in HFD-fed mice.Male C57BL/6 mice were intravenously treated with Ad vectors via the tail vein and were simultaneously fed HFD. PBS-treated mice were fed ND throughout the experimental period. Two weeks after administration of Ad-LPL, Ad-Luc, or PBS, (A, C) expression of mitochondrial genes in the liver determined using quantitative RT-PCR. The data were normalized to the corresponding values in the Ad-Luc-treated group. One-way ANOVA with Dunnett’s post hoc tests was used for multiple comparisons. Hepatic (B) citrate synthase protein levels in male C57BL/6 mice 2 weeks after administration of Ad-LPL or Ad-Luc determined using western blot analysis. The quantification data were normalized to the corresponding value in the Ad-Luc-treated group. The Mann–Whitney U test was used to compare the differences between two independent groups. (D) The area of mitochondria in the liver was assessed via transmission electron microscopy analysis. Arrowheads indicate mitochondria. Bar = 5 µm. (E) The area of mitochondria was determined by measuring the area of mitochondria in the cell using Fig 4D. The Mann–Whitney U test was used to compare the differences between two independent groups. The data are expressed as the mean ± standard error (A–C: n = 5, E: n = 151–155). *, P < 0.05 vs. Ad-Luc.