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 [
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Figure 3Macrophage-specific PPARγ gene deletion causes impaired insulin signaling and lipid accumulation in skeletal muscle and liver. Skeletal muscle (quadriceps) and liver samples were harvested from BMT MAC-WT (
n = 6; white bars) and BMT MAC-KO (
n = 6; black bars) mice following the glucose clamp, and homogenates were immunoprecipitated and immunoblotted for the quantification of IRS-1 tyrosine phosphorylation (
A) as well as for Akt1/2 (Ser473), (
C) IKK-α/β (Ser180/181), and (
D) JNK (Thr183/Tyr185) phosphorylation relative to protein content (
B). Muscle and liver samples were also dehydrated and analyzed for the accumulation of lipid intermediates including diacylglycerol (DAG), long-chain fatty acyl-CoA (LCFACoA) (
E), and triacylglycerol (
F). All values are expressed as a mean ± SEM. Mean differences were detected using 1-way ANOVA; *
P < 0.05.
