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 5
Loss of PPARγ causes macrophage activation and secretion of insulin resistance producing molecules. Altered expression of ABCG1 (A), MCP-1 (B), Cxcl14 (C), and retnla (D) in TG-Mφ from NC-fed BMT MAC-KO (n = 9; black bars) versus BMT MAC-WT (n = 9; white bars) mice. (E) TG-Mφ showing advanced stress fiber formation in the BMT MAC-KOs (NC-fed). Impaired insulin-stimulated 2-deoxyglucose uptake into L6 myocytes incubated with CM from vehicle- (Veh-) or FFA-treated TG-Mφ harvested from BMT MAC-KO (n = 6) versus BMT MAC-WT (n = 6) mice (F and G) and increased GFP-labeled BM-derived cells in skeletal muscle from mice fed a HFD (black bar) versus NC (white bar) (H). Values for RT-PCR are expressed as mean ± SEM. *P < 0.05 between genotypes. Insulin-stimulated 2-DOG assays represent 6 wells per condition and are expressed as mean ± SEM in cpm/μg of protein for absolute tracer uptake values (F) and uptake expressed above basal (G). *P < 0.05, BMT MAC-WT versus BMT MAC-KO, within incubation condition; ^†P < 0.05, vehicle versus FFA, within genotype. (H) GFP immunoblots were quantified using densitometric analysis, and mean expression values ± SEM are presented. n = 4 per group. **P < 0.05 between dietary groups. (I) Immunohistochemical detection shows increased CD11c- and F4/80-expressing cells in skeletal muscle following 8 weeks of high-fat feeding.