Figure 5: HO-1 prevents HFD-induced Akt2 signaling in visceral adipose precursor cells.

(A) pAKT2(S474) and total AKT2 levels were measured by immunoblotting of bead purified viAPs from Hmox1fl/fl and Hmox1fl/flPdgfraCre mice fed either SD or HFD for 3 days. A representative western blot is shown. The experiment was repeated at least three times. (B) Quantification of the pAKT2(S474)/AKT2 ratio. (C,D) Oxygen consumption rates (OCR) and mitochondrial function of viAPs derived from Hmox1fl/fl and Hmox1fl/flPdgfraCre mice (n = 4). (E,F) Oxygen consumption rates (OCR) and mitochondrial function of viAPs derived from Hmox1fl/fl and Hmox1fl/flPdgfraCre mice. N-acetyl-cysteine (NAC, 10 μM) was added 1 hr before measurements (n = 4). (G) Flow cytometric quantitation of mitoSOX-stained viAPs derived from Hmox1fl/fl and Hmox1fl/flPdgfraCre mice (n = 6). (H) NBT reduction staining of viAPs derived from Hmox1fl/fl and Hmox1fl/flPdgfraCre mice, after 48 hrs in culture (n = 4). (I–J) Oxygen consumption rates (OCR) and mitochondrial function of viAPs derived from Hmox1fl/fl and Hmox1fl/flAdipoQCre mice (n = 4). Results are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001.