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. 2014 Nov 13;63(12):4172–4185. doi: 10.2337/db14-0026

Figure 2.

Figure 2

Deletion of MPO diminishes HFD-induced obesity via upregulation of UCP1 and mitochondrial oxygen consumption in BAT. A: MPO−/− and WT mice were fed the ND or HFD for 16 weeks. After thioglycollate treatment, neutrophils were isolated, and expression of MPO was determined by Western blotting. B: Neutrophils were isolated from WT and MPO−/− mice fed the ND or HFD, and peroxidase activity was assayed (n = 4). *P < 0.05 vs. ND-fed WT. RLU, relative luminescence units. C: Weight gain in WT and MPO−/− mice fed the ND or HFD (n = 8–10). *P < 0.05 vs. ND-fed WT; †P < 0.05 vs. HFD-fed WT. D: Fat pad weight in WT and MPO−/− mice fed the HFD for 16 weeks. *P < 0.05 vs. WT. E: Rectal temperature of WT and MPO−/− mice fed the HFD for 16 weeks (n = 8). *P < 0.05 vs. WT. Levels of UCP1 (F) and UCP3 (G) mRNA in BAT from WT and MPO−/− mice fed the HFD for 16 weeks were measured by quantitative real-time PCR. *P < 0.05 vs. WT. H: Protein levels of UCP1 and UCP3 in BAT isolated from HFD-fed WT and MPO−/− mice were measured by Western blotting. I: UCP1 level was quantified by densitometry. *P < 0.05 vs. WT. J: Mitochondrial oxygen consumption in HFD-fed WT and MPO−/− mouse BAT was measured after stimulation with succinate and ADP (n = 3). *P < 0.05 vs. WT. K: BAT mitochondrial fractions were treated with succinate and ADP, and ATP production was assayed by high-performance liquid chromatography. L–N: BAT mitochondria were isolated from HFD-fed WT and MPO−/− mice, and oxygen consumption rates were measured as described in research design and methods (n = 4). *P < 0.05 vs. WT. AM+Ro, antimycin A + rotenone; Pal. CoA, palmitoyl CoA.