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. 2012 Feb 1;26(3):259–270. doi: 10.1101/gad.180406.111

Figure 3.

Figure 3.

Hif1α inactivation in visceral WAT promotes Pgc1α target gene expression and mitochondrial biogenesis. (A) Gene expression profiling of visceral WAT of Hif1α iC(T) and Hif1α icKO(T) mice maintained on the HFD/HFD protocol for regulators FAO and mitochondrial biogenesis. All values were normalized internally to 18S RNA expression and to the Hif1α iC(T) control, respectively. (*) P < 0.01 compared with control, set at 1.0. Data are mean ± SEM of values from five mice per group. (B,C) Visceral WAT (B) and BAT (C) biopsies of Hif1α iC(T) and Hif1α icKO(T) maintained on the HFD/HFD protocol were probed for protein expression of VDAC, SDHA, and Cpt1. Sample loading was normalized to β-actin. (D) Quantification of mitochondrial DNA content relative to nuclear DNA content in visceral WAT and BAT. All values were normalized to the Hif1α iC(T) control, respectively. (*) P < 0.05 compared with control, set at 1.0. Data are mean ± SEM of values from four to five mice per group. (E) Visceral WAT sections of Hif1α iC(T) and Hif1α icKO(T) mice maintained on the HFD/HFD protocol were stained for the mitochondrial marker cytochrome oxidase (COX, red), BODIPY (green), phalloidin (pink), and DAPI (blue) and analyzed by immunofluorescence confocal microscopy.