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