Figure 5.

AMPKα1 mediated the inhibition of l-lactate on macrophage M1 polarization. The 6-week-old male mice were divided into four groups, including LS, LL, HS, and HL groups. A, immunoblots for phosphorylation level of AMPKα1 in EATs. B, immunoblots for phosphorylation level of AMPKα1 in ATMs from EATs. BMDMs were treated with vehicle, l-lactate, or AICAR, and then LPS was added. Compound C was used as an AMPK inhibitor. C, immunoblots for phosphorylation level of AMPKα1. D and E, flow cytometry analyses of M1 surface marker CD38 (D) and CD274 (E). F, the mRNA levels of proinflammatory genes. Data are presented as means ± SD of eight mice per group in vivo, four parallel cell samples per group in ATMs, and six parallel cell samples per group in BMDMs, one-way ANOVA with Mann–Whitney test for mice and two-tailed Student’s t test for cell samples; ∗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; ATM, adipose tissue macrophage; BMDM, bone marrow–derived macrophage; CC, compound C; EAT, epididymal adipose tissue; HL, HFD-lactate (i.p.); HS, HFD-saline (i.p.); Lac, l-lactate; LL, LFD-lactate (i.p.); LPS, lipopolysaccharide; LS, LFD-saline (i.p.).