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1.
Figure 8

Figure 8. Effects of neuronal PPARδ deletion on hypothalamic PPARγ and PPARα expression.. From: Neuron-Specific Deletion of Peroxisome Proliferator-Activated Receptor Delta (PPAR?) in Mice Leads to Increased Susceptibility to Diet-Induced Obesity.

Hypothalamic mRNA expression of PPAR isoforms in f/f and KO mice fed LFD or HFD for 33 weeks was assessed by quantitative real-time PCR. Changes in PPARδ, PPARγ and PPARα were normalized to endogenous RPL13A levels and expressed relative to that of the f/f LFD group. Values represent group mean±SEM (n = 6–7). Statistical significance is designated a (p<0.05, f/f vs. KO, same diet) or b (p<0.05, LF vs. HF, same genotype), as determined by two-way ANOVA and Bonferroni post test.

Heidi E. Kocalis, et al. PLoS One. 2012;7(8):e42981.
2.
Figure 6

Figure 6. White adipose tissue hypertrophy and inflammation.. From: Neuron-Specific Deletion of Peroxisome Proliferator-Activated Receptor Delta (PPAR?) in Mice Leads to Increased Susceptibility to Diet-Induced Obesity.

(A) Light micrographs (×10 magnification) of H&E stained slides of WAT from f/f and KO mice fed chow or HFD for 33 weeks. Arrows point to crown-like structures (CLS), of areas of macrophage infiltration and inflammation. (B) Quantification of CLS (CLS/10× field, n = 4) corresponding to inflammatory macrophage infiltration around adipocytes in f/f and KO mice fed either a chow diet or a HFD. Adipose gene expression of inflammatory cytokine (C) TNFα and adipogenesis markers (D) PPARγ and (E) LPL measured by RT PCR. Target gene mRNA levels were normalized to endogenous RPL13A levels. Values are represented as group mean ± SEM relative to the f/f LF group. Statistical significance is designated as b (p<0.05, LF vs. HF same genotype), as determined by two-way ANOVA and Bonferroni post test.

Heidi E. Kocalis, et al. PLoS One. 2012;7(8):e42981.
3.
Figure 5

Figure 5. Gene-diet interactions determine hypothalamic inflammatory signaling and gene expression in neuronal PPARδ KO mice.. From: Neuron-Specific Deletion of Peroxisome Proliferator-Activated Receptor Delta (PPAR?) in Mice Leads to Increased Susceptibility to Diet-Induced Obesity.

Protein and mRNA were isolated from bisected sections of mediobasal hypothalamus of f/f and KO mice fed LFD or HFD for 33 weeks. (A) Total hypothalamic protein extracts were subjected to Western blot analysis using an antibody directed against IκBα. Levels of β-tubulin were determined and used as a loading control. Densitometery of blots yielded relative intensity of protein levels (n = 6). Insert of A shows a representative Western blot. Hypothalamic mRNA levels of (B) IκBα and inflammatory cytokines (C) IL-6 and (D) IL-1β in f/f and KO mice measured by RT-PCR after the study period. Target gene mRNA levels were normalized to endogenous RPL13A levels. Values are represented as group mean ± SEM relative to the LF f/f control group. Statistical significance is designated by a (p<0.05, f/f vs. KO, same diet) or b (p<0.05, LF vs. HF, same genotype), as determined by two-way ANOVA and Bonferroni post test.

Heidi E. Kocalis, et al. PLoS One. 2012;7(8):e42981.
4.
Figure 3

Figure 3. Neuronal PPARδ deletion leads to increased susceptibility to diet induced obesity.. From: Neuron-Specific Deletion of Peroxisome Proliferator-Activated Receptor Delta (PPAR?) in Mice Leads to Increased Susceptibility to Diet-Induced Obesity.

Growth curves of f/f and KO mice fed LFD or HFD for 33 weeks (age 5–38 weeks). Body weight (BW) and body composition (fat and lean mass) were measured at the indicated ages by MRI/NMR. (A) BW curves, (B) lean mass curves, (C) fat mass curves. Susceptibility to diet-induced obesity was measured by two-way repeated measures ANOVA over the experimental period (*, p<0.05, f/f mice fed LF vs. HF diet) and (#, p<0.05, KO mice fed LF vs. HF diet). Total weight gain over the experimental period for (D) body weight gain, (E) lean mass gain, (F) fat mass gain are shown for f/f and KO mice. (G) Cumulative food intake (kcal) of f/f and KO groups fed either LF or HF diets for 33 weeks, determined from bi-weekly measurements of food intake in genotype matched, group housed mice. Feed efficiency of f/f and KO mice fed (H) LFD and (I) HFD is the ratio of weight gained (BW, fat and lean) to that of calories consumed over the entire study period. Values represent the mean±SEM. Statistical significance is denoted by a (p<0.05, f/f vs. KO, same diet) or b (p<0.05, LF vs. HF, same genotype), as determined by one-way ANOVA and Bonferroni post test, or by * (p<0.05 vs. f/f controls), when determined by two-tailed student's t test.

Heidi E. Kocalis, et al. PLoS One. 2012;7(8):e42981.
5.
Figure 4

Figure 4. Effects of dietary fat and PPARδ deletion on brain lipids, fatty acid composition and lipid metabolism genes.. From: Neuron-Specific Deletion of Peroxisome Proliferator-Activated Receptor Delta (PPAR?) in Mice Leads to Increased Susceptibility to Diet-Induced Obesity.

(A) Total levels of triglyceride (TG), diglyceride (DG) and free fatty acid (FFA) extracted from total lipids from brains of f/f and KO mice fed LFD or HFD for 33 weeks (n = 6–7). Composition of individual FFA species making up the (C) FFA and (E) TG fractions were determined by GC-MS analysis, normalized to brain tissue mass (ng/mg tissue) and shown as group mean±SEM. (B) Changes in hypothalamic mRNA levels of target genes involved in (B) lipid uptake and storage (LPL, CD36, GPAT and DGAT), (D) lipid synthesis (FAS, ACC, SCD) and (F) fatty acid oxidation (ACO, PDK4, CPT1A, UCP2) were assessed by quantitative real-time PCR. Gene expression levels were normalized to endogenous RPL13A levels and are expressed as group mean±SEM relative to the level of the f/f LF diet control group. Statistical significance is designated as a (p<0.05, f/f vs. KO, same diet) or b (p<0.05, LF vs. HF, same genotype), as determined by one-way ANOVA and Bonferroni post test.

Heidi E. Kocalis, et al. PLoS One. 2012;7(8):e42981.
6.
Figure 2

Figure 2. Neuronal PPARδ deletion leads to leptin insensitivity.. From: Neuron-Specific Deletion of Peroxisome Proliferator-Activated Receptor Delta (PPAR?) in Mice Leads to Increased Susceptibility to Diet-Induced Obesity.

(A) Food intake in chow fed f/f and KO mice after receiving a bolus injection of leptin (5 mg/kg BW, i.p.) or vehicle (saline) at the onset of the dark period. Mice were housed individually and food intake was measured over 24 hours (n = 10–12). (B) Hypothalamic total protein extracts from f/f and KO mice treated with leptin (5 mg/kg BW i.p.) or vehicle for 30 minutes were used for Western blot analysis to detect levels of STAT3 phosphorylation (Y705). Total STAT3 levels were determined and used as a loading control. Densitometery of blots yielded relative intensity of protein levels, which are expressed as an activation index (pSTAT3/total STAT3) and represented as the group mean ±SEM (n = 4–6) relative to the f/f saline group. (C) Epigonadal fat pad mass and (D) plasma leptin levels of aged matched, chow fed f/f and KO mice represent basal phenotype of these mice. Values represent the mean ± SEM. Statistical significance is denoted in A and B as * (p<0.05 leptin (gray bars) vs. vehicle (white bars) treated groups within each mouse genotype) or # (p<0.05, KO vs. f/f mice treated with leptin), and in panels C and D as * (p<0.05 vs. f/.f controls, two-tailed student's t test).

Heidi E. Kocalis, et al. PLoS One. 2012;7(8):e42981.
7.
Figure 1

Figure 1. Neuronal PPARδ knockdown and brain morphology.. From: Neuron-Specific Deletion of Peroxisome Proliferator-Activated Receptor Delta (PPAR?) in Mice Leads to Increased Susceptibility to Diet-Induced Obesity.

(A) PPARδ gene expression in mediobasal hypothalamus of control (f/f), heterozygous KO (het) and homozygous KO (KO) PPARδ mice. Target gene PPARδ mRNA expression was measured by RT PCR and normalized to endogenous levels of the housekeeping gene RPL13A. (B) Representative Western blot of PPARδ protein levels in total cellular protein extracts from mediobasal hypothalamus of f/f and KO mice. β-tubulin was used as a loading control. (C) Quantification of PPARδ mRNA expression in peripheral and CNS tissues of f/f and KO mice (muscle, liver, white adipose tissue (WAT), brown adipose tissue (BAT), cerebral cortex and hypothalamus). Gene expression was measured by RT PCR and normalized to endogenous levels of the housekeeping gene RPL13A (n = 4–8). (D) Photomicrographs of Nissl staining in brains from f/f, nestin cre+ control and KO mice. Representative sections shown at the level of the hippocampus (top) and hypothalamus (bottom). No obvious differences or malformations in the structure of these or any other forebrain nuclei were observed across genotypes. Scale bar = 500 µm. Values in panels A and C represent the genotype group mean ± SEM, expressed relative to the levels of the f/f control group. Statistical significance is designated as * (p<0.05, vs. f/f control group, ANOVA or two-tailed student's t test).

Heidi E. Kocalis, et al. PLoS One. 2012;7(8):e42981.
8.
Figure 7

Figure 7. Neuronal PPARδ deletion alters hypothalamic neuropeptide gene expression and compensatory hyperphagia after prolonged fasting.. From: Neuron-Specific Deletion of Peroxisome Proliferator-Activated Receptor Delta (PPAR?) in Mice Leads to Increased Susceptibility to Diet-Induced Obesity.

Hypothalamic mRNA levels of neuropeptides in f/f and KO mice fed LFD or HFD for 33 weeks (n = 6–7). Target gene mRNA levels of (A) NPY and (B) POMC were assessed by quantitative RT PCR. (C–D) Fasting induced changes in hypothalamic neuropeptide mRNA levels of f/f and KO mice maintained on a chow diet or fasted for 24 hours. Target gene mRNA levels of (C) NPY, (D) POMC and (E) UCP2 in fed and fasted mice were normalized to RPL13A and are expressed relative to the f/f, fed control. (F) Refeeding after fasting was measured for an additional 24 hours in a separate cohort of individually housed chow fed mice (n = 6–7). Graph shows food intake normalized to basal, pre-fast lean mass (kcal/g lean mass). (G) Percent changes in body weight after a 24 hour fast, after fasting and refeeding for 24 hours, or an additional 7 days. Values represent the mean ± SEM. Statistical significance in panel A–E is designated as a (p<0.05 f/f vs. KO, same diet) or b (p<0.05, LF vs. HF, same genotype), as determined by two-way ANOVA and Bonferroni post test, and in F and G by * (p<0.05 vs. f/f), as determined by two-tailed student's t test.

Heidi E. Kocalis, et al. PLoS One. 2012;7(8):e42981.

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