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. 2020 Feb 12;24(6):3611–3624. doi: 10.1111/jcmm.15053

Figure 7.

Figure 7

Inhibition of P53 ameliorated metabolic reprogramming and insulin resistance induced by palmitate acid. A, The AML12 cells were treated with 0, 5, 10, 20 and 40 μmol/L Pifithrin‐α hydrobromide (PFT) for 24 h, and the protein level of PANK1 was measured by Western blotting. B, The mature miR‐107 was measured by real‐time RT‐PCR. C, Glucose production measured in AML12 cells. D and E, The AML12 cells were treated with or without PFT (20 μmol/L) in the presence of palmitate acid (600 μmol/L) for 24 h. The protein levels of FASN, SCD1, Cpt1α, Cav1 and IRβ in AML12 cells were measured. F, Before harvest, cells were stimulated with 100 nmol/L insulin for 20 min and protein expressions of p‐Akt (S473) and Akt were measured. G, Representative images of Oil Red O staining are shown (400×). H, Proposed mechanisms by which high‐fat diet–induced metabolic reprogramming and insulin resistance through P53 activation of PANK1 and miR‐107, respectively. All values are presented as mean ± SEM. Data in A and B, *P < .05, **P < .01, ***P < .001 (vs CON). Data in C‐F, *P < .05, ***P < .001 (vs CON); # P < .05, ## P < .01, ### P < .001 (vs PA). n = 3 independent experiments