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. 2015 Apr 13;10(4):e0122024. doi: 10.1371/journal.pone.0122024

Fig 6. TNK promotes the deacetylation of PGC1α and FOXO1 and activates AMPK signaling.

Fig 6

Acetylation levels of PGC1α in the skeletal muscle (A) and WAT (B) and FOXO1 acetylation level in the skeletal muscle (C) of SHR/cp rats treated with 3.24 g/kg TNK for 7 weeks are shown. Phosphorylation levels of AMPKα in the liver (D), skeletal muscle (E) and WAT (F) of SHR/cp rats treated with TNK for 7 weeks are shown. Phosphorylation levels of ACC in the liver (G), skeletal muscle (H) and WAT (I) of SHR/cp rats treated with TNK for 7 weeks relative to β-actin. Data are shown as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001 vs. CON. TNK, Tang-Nai-Kang; SHR/cp, SHR.Cg-Lepr cp/NDmcr rat; WKY, Wistar Kyoto rat; CON, control group; TL, low-dose TNK group (1.67 g/kg); TH, high-dose TNK group (3.24 g/kg); WAT, white adipose tissue; PGC1α, peroxisome proliferator activated receptor-γ coactivator 1α; FOXO, forkhead transcription factor; AMPK, AMP-activated protein kinase; ACC, acetyl-CoA carboxylase.