Increased CD36 protein as a response to defective insulin signaling in macrophages
J. Clin. Invest. Chien-Ping Liang, et al. 113:764 doi:10.1172/JCI19528 [Go to this article.]

Figure 4
Short-term treatment with insulin or PI3 kinase inhibitors, or long-term treatment with glucose or fatty acids, does not increase CD36 protein expression in WT macrophages. (A–D) Pooled WT macrophages (A, B, and D) or WT and ob/ob monocytes (C) isolated from three to ten mice were incubated with insulin (1 μM) for 0.5 hours or with the PI3 kinase inhibitors wortmannin (200 nM) or LY294002 (20 μM) for 2 hours (A), with glucose or mannitol at the indicated concentrations for 2 days (B), with 400 mg/dl of glucose or mannitol for 1 day (C), or with oleic acid– or palmitic acid–BSA complexes for 1 day (D). Troglitazone (TRG; 1 μM) was used as a positive control. Treated cells were then used for oxLDL binding assays with the SR-A ligand fucoidan (50 μg/ml) added to the binding buffer or for total protein extraction followed by Western analysis. One experiment representative of two (A, B, and D) or three (B) independent experiments is shown. Mφ, macrophage; FA, fatty acid; Conc., concentration.