Fig 2: EA increased WAT-browning related proteins in IWAT of HFD + EA group but not in HFD group. SIRT-1 (A, B), PRDM16 (C, D), and p-AMPK (E, F) expression in IWAT obtained from ND-fed, HFD-fed or HFD + EA-fed rats following 14 weeks of treatment. Data were represented as mean ± SD (n = 3). ##P < 0.01 vs. the ND group, *P < 0.05 vs. the HFD + EA group.

Fig 3: EA treatment facilitated the interaction between PPARγ and PRDM-16 and decreased PPARγ and PGC-1α acetylation. IWAT tissues from ND, HFD and HFD + EA groups were immunoprecipitated with acetylated lysine (AcK) antibody and immunoblotted with PPARγ and PGC-1α antibodies. (A) Western blot for Co-IP studies of PPARγ and PRDM16. (B) Acetylation of PPARγ and PGC-1α in white adipose tissue. The ratios of acetylated PPARγ to PPARγ (C) and acetylated PGC-1α to PGC-1α (D). Data were represented as mean ± SD (n = 3). ##P < 0.01 vs. the ND group; **P < 0.01 vs. the HFD + EA group.

Fig 4: The mRNA expression of PGC1α and PRDM16 in back and abdominal fat tissues between the surviving and dead piglets. a-b, The relative mRNA levels of PGC1α and PRDM16 were elevated in both fat pads in surviving piglets compared to the dead piglets. *P < 0.05, n = 10

Fig 5: LINC00589-dominated regulatory networks in breast cancer patients’ tissues.A–D mRNA expression of LINC00589, miR-100, miR-452, DLG5, and PRDM16 of the dissected tissues from 71 patients were measured by qRT-PCR assay. The correlation of LINC00589-miR-100 (A), LINC00589-miR-452 (B), miR-100-DLG5 (C), and miR-452-PRDM16 (D) were analyzed by the Spearman correlation test. E Protein expression of DLG5 and PRDM16 were analyzed by immunohistochemistry (IHC) in tissues from trastuzumab-responding or non-responding patients. Scale bar 50 μm.