Extended Data Fig. 4: White adipocyte mitochondrial hyperactivity following CKB silencing is not driven by fatty acid oxidation or glutaminolysis. | Nature Metabolism

Extended Data Fig. 4: White adipocyte mitochondrial hyperactivity following CKB silencing is not driven by fatty acid oxidation or glutaminolysis.

From: Impaired phosphocreatine metabolism in white adipocytes promotes inflammation

Extended Data Fig. 4

a-b. CCL2 expression in in vitro differentiated human adipocytes transfected with either siC or siCKB, and treated with 3 μmol/L Etomoxir (fatty acid oxidation inhibitor) (three replicates/condition) (A) or 10 μmol/L BPTES (glutaminolysis inhibitor) (four replicates per condition) (B). Control cells were treated with DMSO. Data are shown as mean ± SEM. Overall p < 0.0001 for panel A and 0.028 for panel B by one-way ANOVA. Results from Tukey’s post-hoc test are indicated by *p < 0.05, ***<0.001 and ****p < 0.0001, respectively. Abbreviations: BPTES = Bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl)ethyl sulfide, DMSO = dimethyl sulfoxide.

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