Article Figures & Data
Figures
- Figure 1.
Effects of HFD on body composition and glucose tolerance. A, ADP-KO and WT mice fed HFD were assessed for body weight, fat content and lean mass, shown as mean ± SE (n = 10 per group). **p < 0.01; ***p < 0.001. B, Blood glucose measurements before and after a glucose challenge are shown as mean ± SE (n = 9–10 per group; genotype p = 0.0164, time p < 0.0001, interaction p = 0.281). Post hoc analysis revealed significantly differences at times 0 (p = 0.049), 60 min (p = 0.0213) and 120 min (p = 0.0135).
- Figure 2.
Kainic acid seizure in mice fed HFD. A, Data are mean ± SE; n = 6. ADP-KO mice exhibited higher seizure scores (genotype p = 0.0127, time p < 0.0001, interaction p < 0.0001). Post hoc analysis with Bonferroni's correction revealed higher seizure scores from 60 min to 105 min (p < 0.01 to p < 0.001). B, Brain sections were stained with cresyl violet (top), or for GFAP (middle), and Iba1 (bottom). Representative images of hippocampus are shown, with higher-power images of the dentate gyrus endplate shown in the insets. Hippocampal regions are labeled for reference. Scale bars: Top and middle, 500 μm; bottom, 100 μm; inset, 50 μm. C, Semiquantitative pathology scores, shown as mean ± SE; n = 6. Dashed line denotes baseline normal score of 1 (**p < 0.01, ***p < 0.001). D, Neurodegeneration and gliosis in a kainic acid-treated ADP-KO mouse. Cresyl violet (left and middle)- and Iba1 (right)-stained sections are shown. Boxed region is CA1. Arrowhead points to a pyknotic neuron in contrast with viable neuron (asterisk). Scale bars: left, 500 μm; middle, 50 μm; right, 100 μm.
- Figure 3.
Intrahippocampal kainic acid and seizure-related pathology. A, Hippocampal sections were stained with cresyl violet (top, at low and high magnification), or for GFAP (middle, at low and high magnification), Iba1 (middle, at low magnification), and synaptophysin (SYN; bottom, at high magnification). Scale bars: lower-magnification panels, 500 μm; higher-magnification panels, 50 μm. DG, Dentate gyrus; CA3, cornu ammonis 3; H, hilum. B, Dentate gyrus thickness measurements shown as mean ± SE with dashed line denoting normal thickness. C–E, Semiquantitative pathology scores, shown as mean ± SE; n = 4–6. Dashed line denotes normal baseline score of 1. *p < 0.05 for genotype by two-way ANOVA).
Tables
Triglyceride (mg/dl) NEFA (mEq/L) Cholesterol (mg/dl) WT saline 27.0 ± 1.4 0.787 ± 0.022 134.0 ± 8.3 WT kA 35.5 ± 2.7 0.762 ± 0.043 121.3 ± 4.7 KO saline 42.9 ± 3.4 0.926 ± 0.016 173.5 ± 8.6 KO KA 49.7 ± 8.5 0.866 ± 0.076 146.9 ± 8.4 Two-way ANOVA Genotype 0.019 0.047 0.0006 Treatment 0.202 0.462 0.020 Interaction 0.892 0.764 0.375 Data are shown as mean ± SE (n = 4–6 per group). Two-way ANOVA results are shown with significant p values in bold.
In this issue
