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. 2021 Feb 1;8(6):2002794. doi: 10.1002/advs.202002794

Figure 6.

Figure 6

AKAP1 deficiency increases mitochondrial thermogenesis in brown adipocyte by enhancing fatty acid β‐oxidation and subsequent UCP1 upregulation. a) OCR measurement in differentiated WT and AKAP1−/− brown adipocytes pretreated with 500 µM palmitate for 24 h. During measurement, brown adipocytes were sequentially stimulated with the following compounds: 1 µM Norepinephrine (NE), 3 µM Oligo, and 4 µM each of AA/R. Basal OCR corresponds to baseline OCR minus AA/R‐insensitive OCR; NE‐dependent OCR corresponds to NE addition phase OCR minus Basal OCR. Leak OCR corresponds to Oligo‐insensitive OCR minus AA/R‐insensitive OCR. Data were from three independent experiments. b) UCP1 mRNA and protein expression in differentiated WT and AKAP1−/− brown adipocytes pretreated with 500µM palmitate for 24 h. Data were from three independent experiments. c) OCR measurement in differentiated AKAP1−/− brown adipocytes with siRNA transfection. Data were from three independent experiments. d) UCP1 mRNA and protein expression in differentiated AKAP1−/− brown adipocytes with siRNA transfection. Data were from three independent experiments. e) OCR measurement in differentiated WT and AKAP1−/− brown adipocytes with Eto treatment. Dimethyl sulfoxide (DMSO) was used as control. Data were from three independent experiments. f) UCP1 mRNA and protein expression in differentiated AKAP1−/− brown adipocytes with Eto treatment. Data were from three independent experiments. Data were expressed as mean ± SEM. Student's t‐test was used in (a–f). *p < 0.05, **p < 0.01.