Fig. 3: Adipocyte CK-B regulates CCL2 expression by modulating mitochondrial energy production.

a, Normalized OCR determined in human adipocytes transfected with scrambled non-silencing (siC) or CKB-targeting (siCKB) oligonucleotides (12 replicates per condition, repeated three times). Non-mitochondrial respiration was substracted from the basal and maximal respiration is represented in the bar chart. **P = 0.0059, ***P = 0.0008, ****P < 0.0001 (both basal and maximal respiration). O, Oligomycin; F, FCCP; R/A, rotenone/antimycin. b, Mitochondrial ATP production based on Seahorse data in human adipocytes transfected with siC or siCKB (n = five replicates per condition, repeated twice). **P = 0.0078. c, ATP/ADP ratio measured by bioluminescence in human adipocytes transfected with siC or siCKB (nine replicates per condition, repeated twice). ****P < 0.0001. d, Schematic representation of drugs targeting mitochondrial ATP production and/or substrate usage. e, Effect of the mitochondrial inhibitors 1 μM oligomycin (O) or 1 μM bongkrekic acid (B) for 24 h on ATP/ADP ratio in human adipocytes transfected with siC or siCKB. Control wells were treated with dimethyl sulfoxide (DMSO) (D) (five replicates per condition, repeated twice). Overall P = 0.043. f, Same experimental setup as e but displaying CCL2 mRNA expression (four replicates per condition, repeated twice). Overall P = 0.0003. g, Same experimental setup as in e but displaying CCL2 secretion (pg ml⁻¹) detected by ELISA (four replicates per condition, repeated twice). Overall P < 0.0001. Data were analysed by Student’s two-sided t-test in a–c and by one-way ANOVA in e–g (Tukey’s post-hoc tests indicated by *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001). Data are shown as mean ± s.e.m. 2DG, 2-deoxy-D-glucose; ANT,adenine nucleotide translocase; a.u., arbitray unit; CPT1, carnitine palmitoyl transferase 1; FA, fatty acid; GLS, glutaminase; MPC1, mitochondrial pyruvate carrier 1.