Macrophage PPARγ is required for normal skeletal muscle and hepatic insulin sensitivity and full antidiabetic effects of thiazolidinediones
J. Clin. Invest. Andrea L. Hevener, et al. 117:1658 doi:10.1172/JCI31561 [Go to this article.]

Figure 2
Macrophage-specific PPARγ gene deletion causes glucose intolerance and skeletal muscle and hepatic insulin resistance. GTTs were performed following a 6-hour fast in 12-month-old MAC-WT (n = 6) versus MAC-KO (n = 7) (A) and 10-month-old BMT MAC-WT (n = 7) versus BMT MAC-KO (n = 10) mice (B). *P < 0.05, mean values for WT (open squares) versus KO (filled squares); repeated-measures ANOVA with Tukey’s post-hoc procedure. Insulin’s ability to stimulate glucose disposal (IS-GDR) into skeletal muscle of 12-month-old MAC-WT (n = 6) versus MAC-KO (n = 7) (C) and 10-month-old BMT MAC-WT (n = 7) versus BMT MAC-KO (n = 10) mice (D). IS-GDR values are expressed as mean ± SEM. Mean differences were detected using 1-way ANOVA. *P < 0.05 between genotypes. Insulin’s ability to suppress HGP was determined in MAC-WT versus MAC-KO (E) and BMT MAC-WT versus BMT MAC-KO (F) mice. HGP values are expressed as mean ± SEM for basal conditions versus clamp. Mean differences between genotypes within condition were detected using 1-way ANOVA. *P < 0.05 between genotypes, within condition.