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. 2022 Feb 24;298(4):101768. doi: 10.1016/j.jbc.2022.101768

Figure 7.

Figure 7

l-lactate activated macrophage AMPKα1 signal to reduce associated adipocyte insulin resistance. BMDMs were treated with vehicle, l-lactate, or AICAR, and then LPS was added. Compound C was used as an AMPK inhibitor. BMDMs conditional media were collected after 24 h of incubation in the fresh media. A and B, the mRNA levels of TNF-α (A) and MCP1 (B) in 3T3-L1 adipocytes. C, immunoblots for phosphorylated AKT (Ser473) and total AKT in 3T3-L1 adipocytes. D, immunoblots for plasma membrane GLUT4 and total GLUT4 in 3T3-L1 adipocytes. Data are presented as means ± SD of six parallel samples per group, two-tailed Student’s t test; ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001. AICAR, 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside; AMPKα1, AMP-activated protein kinase alpha 1; BMDM, bone marrow–derived macrophage; CC, compound C; CM, conditional media; Con, control; GLUT4, glucose transporter type 4; Lac, l-lactate; LPS, lipopolysaccharide; MCP1, monocyte chemoattractant protein 1; PM, plasma membrane; TNF-α, tumor necrosis factor alpha.