Neuronal PPARδ deletion leads to increased susceptibility to diet induced obesity.

<p>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 (*, <i>p</i><0.05, f/f mice fed LF <i>vs.</i> HF diet) and (#, <i>p</i><0.05, KO mice fed LF <i>vs.</i> 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 (<i>p</i><0.05, f/f <i>vs.</i> KO, same diet) or <i>^b</i> (<i>p</i><0.05, LF <i>vs.</i> HF, same genotype), as determined by one-way ANOVA and Bonferroni post test, or by * (<i>p</i><0.05 <i>vs.</i> f/f controls), when determined by two-tailed student's <i>t</i> test.