Figure 4.

Leptin increases peroxisome proliferator-activated receptor gamma expression and restores endothelial function in congenital generalized lipodystrophy. PPARγ gene expression in thoracic aorta from gBscl2^+/+ or gBscl2^−/− (Berardinelli-Seip 2 gene–deficient) mice treated or not with leptin (10 μg/d for 7 d; osmotic mini-pump) and PPARγ gene expression in pulmonary endothelial cells from endothelial leptin receptor (LepR) wild-type (LepREC^+/+) or deficient (LepREC^−/−) mice (A). PPAR-γ gene expression after metreleptin stimulation (8 or 24 h) in human aortic segments (B) or human umbilical vascular endothelial cells (HUVECs; C); concentration response curves to acetylcholine (ACh) in presence or not of pioglitazone (10 μM; D) and in presence or not of leptin (10 μg/mL) +GW9662 (5 μM; E) in aortic rings from gBscl2^+/+ or gBscl2^−/− mice; pioglitazone preincubation effects (10 μM/2 h) on superoxide production in HUVEC transduced with Nox1/NoxA1/NoxO1 (F). Data are presented as means±SEM. For PPARγ gene expression in mouse samples, Real-time polymerase chain reaction graph is presented as interleaved from minimal to maximal. n=3 to 6. *P<0.05 vs gBscl2^+/+; *P<0.05 vs LepR^EC+/+; †P<0.05 vs Nox1/NoxA1/NoxO1-transduced HUVEC. t test was used for comparison between 2 groups. One-way ANOVA followed by Tukey multiple comparison test was used for comparison between 3 different groups. Two-way ANOVA test followed by Tukey multiple comparison test was used for comparison between 4 groups.