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Fig. 5 | BMC Biology

Fig. 5

From: PPARα is essential for retinal lipid metabolism and neuronal survival

Fig. 5

Diminished mitochondrial function in Pparα -/- retinas. ad Basal and maximal mitochondrial oxygen consumption rate (OCR) were decreased in (a, b) 8-week-old and (c, d) 12-week-old Pparα -/- retinas relative to age-matched wild-type (WT) controls (WT 8 weeks, n = 17; Pparα -/- 8 weeks, n = 20; WT 12 weeks, n = 21; Pparα -/- 12 weeks, n = 15). e Retinal NADH oxidation was decreased in Pparα -/- retinas relative to age-matched WT controls beginning at 8 weeks of age (8 weeks WT, n = 10; Pparα -/-, n = 9; 18 weeks, n = 6/genotype; 60 weeks, n = 3/genotype). f Retinal NADH oxidation was decreased in 11-week-old Vldlr -/- retinas and restored by treatment with PPARα agonist fenofibric acid (Feno) (WT Veh, n = 7; WT Feno-FA, n = 8; Vdllr -/- Veh, n = 7; Vdllr -/- Feno-FA, n = 8). g Transmission electron microscopy revealed that at 40 weeks of age, photoreceptor mitochondria had an “active” compressed morphology in WT retinas, and an “inactive” orthodox morphology in Pparα -/- retinas (n = 3/genotype). *P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001; ****P ≤ 0.0001, unpaired two-tailed Student’s t test (ae) or one-way ANOVA with Tukey’s post-hoc comparison (f)

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